IL-1R type I-dependent hemopoietic stem cell proliferation is necessary for inflammatory granulopoiesis and reactive neutrophilia
Open accessAbstract
Infections and inflammation trigger neutrophilias that are supported by a hematopoietic program of accelerated granulopoiesis known as emergency granulopoiesis. The intrinsic factors that drive reactive neutrophilias and emergency granulopoiesis have been inferred but not demonstrated. Here, we show that alum cannot elicit reactive neutrophilias in IL-1R type I (IL-1RI)−/− mice, whereas other inflammatory responses, including eosinophilia and Ab production, remain intact. Analysis of this specific impairment revealed an unanticipated role for IL-1RI in supporting increased proliferation by granulocyte/macrophage progenitors and, surprisingly, multipotent progenitors and hematopoietic stem cells (HSC). Indeed, HSC and multipotent progenitor proliferative responses were most suppressed in IL-1RI−/− mice, suggesting a critical role for their proliferation in inflammatory granulopoiesis. Whereas IL-1 drives increased HSC proliferation directly in vitro, IL-1RI expression by radiation-resistant host cells was both necessary and sufficient for alum-induced HSC, multipotent progenitor, and granulocyte/macrophage progenitor proliferation and reactive neutrophilias in radiation chimeric mice. Thus, IL-1 plays a necessary, but indirect, role in the support of alum-induced neutrophilias by expanding both pluripotent and myeloid progenitor compartments to accelerate granulopoiesis.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
IL-1 can stimulate HSC proliferation, driving their myeloid differentiation at the expense of self-renewal, thus eroding their repopulating capacity.
“Indeed, IL-1 can stimulate HSC proliferation, driving their myeloid differentiation at the expense of self-renewal, thus eroding their repopulating capacity.28,49,50”
From Aging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling (2023) · cites this paper as [49]
The Discussion (page not supplied) reports that HSC proliferate in response to IL-1 in vitro and that IL-1RI-dependent signaling supports HSC proliferation during alum-induced granulopoiesis. It does not establish that this proliferation drives myeloid differentiation at the expense of self-renewal or erodes HSC repopulating capacity; those outcomes are not reported in the passages retrieved. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIL-1 signaling is closely linked to chronic inflammatory diseases and plays a critical role in the activation of inflammatory myelopoiesis.
“IL-1β is produced in response to a wide range of physiological insults, and IL-1 signaling is closely linked to a wide variety of chronic inflammatory diseases, where it plays a critical role in the activation of inflammatory myelopoiesis (Ueda et al., 2009; Dinarello, 2011; Mirantes et al., 2014; Pietras, 2017).”
From PU.1 is required to restrain myelopoiesis during chronic inflammatory stress (2023) · cites this paper as Ueda et al., 2009
The Discussion reports that IL-1RI is indispensable for alum-induced emergency granulopoiesis in mice, supporting a critical role for IL-1 signaling in that inflammatory response. It does not establish the claim’s broader link to a wide variety of chronic inflammatory diseases or show that IL-1 activates myelopoiesis in those diseases. No page number is available in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPublished BM chimera studies show that in vivo HSC proliferation in response to IL-1 can be triggered independently of IL-1 receptor (IL-1R) on HSCs themselves and may rely on IL-1R-induced G-CSF production in the BM niche.
“published BM chimera studies show that in vivo HSC proliferation in response to IL-1 can be triggered independently of IL-1 receptor (IL-1R) on HSCs themselves (Cain et al., 2011; Ueda et al., 2009) and may rely on IL-1R–induced G-CSF production in the BM niche.”
From PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress (2021) · cites this paper as Ueda et al., 2009
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Biologic basis for interleukin-1 in disease.
Dinarello, C. (1996) · Blood · doi:10.1182/blood.v87.6.2095.bloodjournal8762095 · Cited by 3,380 · cited 4× · see citing works
“IL-1 is a potent proinflammatory cytokine and IL-1RI is expressed by many cell types (33), raising the possibility that the absence of alum-induced neutrophilias in IL-1RI-deficient mice is not a specific effect but a general suppression of all inflammatory responses.”
BackgroundInfluentialHornung, V., Bauernfeind, F., Halle, A., Samstad, E. O., Kono, H., Rock, K. L., Fitzgerald, K. A., & Latz, E. (2008) · Nature Immunology · doi:10.1038/ni.1631 · Cited by 3,065 · cited 3× · see citing works
“IL-1 is an important component to inflammatory responses elicited by mineral salts (27) and synergizes with TNF- to increase neutrophil production in BM (21).”
BackgroundA clonogenic common myeloid progenitor that gives rise to all myeloid lineages
Akashi, K., Traver, D., Miyamoto, T., & Weissman, I. L. (2000) · Nature · doi:10.1038/35004599 · Cited by 2,617 · cited 2× · see citing works
“To exclude this possibility, we analyzed LSK cells from naive and immunized mice for expression of Fc RII/III and IL-7R , molecules not expressed by HSC and MPP but characteristic of GMP and common lymphoid progenitors (CLP), respectively (9, 23).”
BackgroundTargeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function.
Adachi, O., Kawai, T., Takeda, K., Matsumoto, M., Tsutsui, H., Sakagami, M., Nakanishi, K., & Akira, S. (1998) · Immunity · doi:10.1016/s1074-7613(00)80596-8 · Cited by 2,358 · cited 1× · see citing works
“(34), showing that the alum’s adjuvanticity is abrogated in mice defective for components of the Nalp3 inflammasome, but intact in animals lacking MyD88, a crucial signaling component of the IL-1 and IL-18 receptors (44).”
BackgroundIdentification of Clonogenic Common Lymphoid Progenitors in Mouse Bone Marrow
Kondo, M., Weissman, I. L., & Akashi, K. (1997) · Cell · doi:10.1016/s0092-8674(00)80453-5 · Cited by 2,253 · cited 5× · see citing works
“HSC, MPP, and GMP (n 500) were cultured with recombinant IL-1 (1 ng/ml; PeproTech) or GM-CSF (1 ng/ml; PeproTech) in X-VIVO15 serum-free medium (Cambrex) containing SCF (25 ng/ml; R&D Systems) to promote HSC survival (24).”
BackgroundMethodResultInfluentialSelf-citationCrucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminium adjuvants
Eisenbarth, S. C., Colegio, O. R., O’Connor, W., Sutterwala, F. S., & Flavell, R. A. (2008) · Nature · doi:10.1038/nature06939 · Cited by 1,542 · cited 5× · see citing works
“Alum drives IL-1 and IL-18 secretion by activating the Nalp3 inflammasome (27, 34, 35), and these cytokines have been proposed to be the agents of alum’s several inflammatory properties including adjuvanticity (34).”
BackgroundInfluentialSouza, L., Boone, T., Gabrilove, J., Lai, P., Zsebo, K., Murdock, D., Chazin, V., Bruszewski, J., Lu, H.-B., Chen, K.-K., et al. (1986) · Science · doi:10.1126/science.2420009 · Cited by 1,286 · see citing works
Identification of Flt3+ Lympho-Myeloid Stem Cells Lacking Erythro-Megakaryocytic Potential
Adolfsson, J., Månsson, R., Buza-Vidas, N., Hultquist, A., Liuba, K., Jensen, C. T., Bryder, D., Yang, L., Borge, O. J., Thorén, L., et al. (2005) · Cell · doi:10.1016/j.cell.2005.02.013 · Cited by 1,229 · see citing works
John, D., & Sugo, Y. (2006) · doi:10.4049/issn.1550-6606 · Cited by 922
Zhang, D.-E., Zhang, P., Wang, N.-D., Hetherington, C. J., Darlington, G. J., & Tenen, D. G. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.2.569 · Cited by 910 · cited 2× · see citing works
“Steady-state and emergency granulopoiesis can be distinguished by separate dependencies on the C/EBP and C/EBP transcription factors (CCAAT enhancer-binding proteins) (6, 11).”
BackgroundChen, C.-J., Kono, H., Golenbock, D., Reed, G., Akira, S., & Rock, K. L. (2007) · Nature Medicine · doi:10.1038/nm1603 · Cited by 876 · cited 1× · see citing works
“The requirement for IL-1RI in alum-induced neutrophilias and emergency granulopoiesis emphasizes the central role of IL-1 in innate immune responses (27, 42, 43).”
BackgroundYamaguchi, Y., Suda, T., Suda, J., Eguchi, M., Miura, Y., Harada, N., Tominaga, A., & Takatsu, K. (1988) · Journal of Experimental Medicine · doi:10.1084/jem.167.1.43 · Cited by 566 · cited 1× · see citing works
“IL-3 and IL-5 promote eosinophilia (36), and”
Chen, C. (2006) · Journal of Clinical Investigation · doi:10.1172/jci28075 · Cited by 475 · cited 1× · see citing works
“The requirement for IL-1RI in alum-induced neutrophilias and emergency granulopoiesis emphasizes the central role of IL-1 in innate immune responses (27, 42, 43).”
BackgroundYang, L., Bryder, D., Adolfsson, J., Nygren, J., Månsson, R., Sigvardsson, M., & Jacobsen, S. E. W. (2004) · Blood · doi:10.1182/blood-2004-06-2159 · Cited by 469 · cited 2× · see citing works
“2) (7) numbers rose to 150% of naive controls, remained elevated through day 4, and then returned to naive levels by day 6 (Fig.”
BackgroundC/EBPβ is required for 'emergency' granulopoiesis
Hirai, H., Zhang, P., Dayaram, T., Hetherington, C. J., Mizuno, S.-I., Imanishi, J., Akashi, K., & Tenen, D. G. (2006) · Nature Immunology · doi:10.1038/ni1354 · Cited by 425 · see citing works
Phenotypic and functional characterization of mice that lack the type I receptor for IL-1.
Glaccum, M. B., Stocking, K., Charrier, K., Smith, J., Willis, C., Maliszewski, C., Livingston, D., Peschon, J., & Morrissey, P. (1997) · Journal of Immunology · doi:10.4049/jimmunol.159.7.3364 · Cited by 418 · see citing works
Absence of IL-1 signaling and reduced inflammatory response in IL-1 type I receptor-deficient mice.
Labow, M., Shuster, D., Zetterström, M., Nunes, P., Terry, R., Cullinan, E., Bártfai, T., Solórzano, C., Moldawer, L., Chizzonite, R., et al. (1997) · Journal of Immunology · doi:10.4049/jimmunol.159.5.2452 · Cited by 376 · cited 1× · see citing works
“The blood of naive BL/6 and IL-1RI / mice contain identical numbers of neutrophils, inflammatory monocytes, and eosinophils (29) (Fig.”
BackgroundGATA-2 Plays Two Functionally Distinct Roles during the Ontogeny of Hematopoietic Stem Cells
Ling, K.-W., Ottersbach, K., van Hamburg, J. P., Oziemlak, A., Tsai, F., Orkin, S., Ploemacher, R., Hendriks, R., & Dzierzak, E. (2004) · Journal of Experimental Medicine · doi:10.1084/jem.20031556 · Cited by 355 · cited 2× · see citing works
“We cultured 100 Flt3 LSK BM cells from naive and immunized (day 2) mice with SCF, IL-3, IL-6, and erythropoietin (32).”
MethodInflammation and the reciprocal production of granulocytes and lymphocytes in bone marrow
Ueda, Y., Kondo, M., & Kelsoe, G. H. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041419 · Cited by 343 · cited 9× · see citing works
“We have observed that alum promotes granulopoiesis at the expense of B lymphopoiesis and have proposed that these lineages compete for developmental resources in the BM (10, 21).”
BackgroundInfluentialSelf-citationAluminum Hydroxide Adjuvants Activate Caspase-1 and Induce IL-1β and IL-18 Release
Li, H., Nookala, S., & Re, F. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.178.8.5271 · Cited by 333 · cited 3× · see citing works
“of the proinflammatory cytokines IL-1 , IL-18, and IL-33 (34, 35).”
BackgroundHuman IL-3 and GM-CSF act synergistically in stimulating hematopoiesis in primates.
Donahue, R., Seehra, J., Metzger, M., Lefebvre, D., Rock, B., Carbone, S., Nathan, D., Garnick, M., Sehgal, P., & Laston, D. (1988) · Science · doi:10.1126/science.3051378 · Cited by 328 · see citing works
Rapid recruitment of inflammatory monocytes is independent of neutrophil migration
Henderson, R. B., Hobbs, J. A. R., Mathies, M., & Hogg, N. (2003) · Blood · doi:10.1182/blood-2002-10-3228 · Cited by 309 · see citing works
Inflammation Controls B Lymphopoiesis by Regulating Chemokine CXCL12 Expression
Ueda, Y., Yang, K., Foster, S. J., Kondo, M., & Kelsoe, G. (2004) · Journal of Experimental Medicine · doi:10.1084/jem.20031104 · Cited by 286 · cited 10× · see citing works
“To determine the role of IL-1RI in reactive neutrophilias, we injected C57BL/6 (BL/6) and congenic IL-1RI / mice with alum/Ag (21) and followed changes in blood leukocyte numbers over 8 days.”
BackgroundMethodInfluentialSelf-citationThe neutrophil: function and regulation in innate and humoral immunity.
Burg, N. D., & Pillinger, M. (2001) · Clinical Immunology · doi:10.1006/clim.2001.5007 · Cited by 286 · cited 3× · see citing works
“those elicited by infection (3, 4); that is, both begin with the mo-”
BackgroundNishinakamura, R., Miyajima, A., Mee, P., Tybulewicz, V., & Murray, R. (1996) · Blood · doi:10.1182/blood.v88.7.2458.bloodjournal8872458 · Cited by 233 · cited 3× · see citing works
“cytokine/receptor pathway for emergency granulopoiesis (5, 20).”
BackgroundCheers, C., Haigh, A., Kelso, A., Metcalf, D., Stanley, E., & Young, A. M. (1988) · Infection and Immunity · doi:10.1128/iai.56.1.247-251.1988 · Cited by 231 · cited 1× · see citing works
“Indeed, microbial infections increase serum GM-CSF and G-CSF coincidentally with the number of myeloid progenitors in BM (13).”
BackgroundDomen, J., & Weissman, I. L. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.192.12.1707 · Cited by 219 · cited 1× · see citing works
“HSC, MPP, and GMP (n 500) were cultured with recombinant IL-1 (1 ng/ml; PeproTech) or GM-CSF (1 ng/ml; PeproTech) in X-VIVO15 serum-free medium (Cambrex) containing SCF (25 ng/ml; R&D Systems) to promote HSC survival (24).”
MethodIdentification of eosinophil lineage–committed progenitors in the murine bone marrow
Iwasaki, H., Mizuno, S.-I., Mayfield, R., Shigematsu, H., Arinobu, Y., Seed, B., Gurish, M. F., Takatsu, K., & Akashi, K. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050548 · Cited by 205 · cited 1× · see citing works
“This observation is consistent with the work of Iwasaki and colleagues, who showed that eosinophilias elicited by helminth infections are supported by expansions of a committed eosinophil progenitor compartment but not CMP or GMP (41).”
ResultCaracciolo, D., Clark, S., & Rovera, G. (1989) · Blood · doi:10.1182/blood.v73.3.666.666 · Cited by 162 · see citing works
“Emergency” granulopoiesis in G-CSF–deficient mice in response to Candida albicans infection
Basu, S., HODGSON, G. S., Zhang, H., Katz, M., Quilici, C., & Dunn, A. R. (2000) · Blood · doi:10.1182/blood.v95.12.3725 · Cited by 144 · see citing works
Layton, J., Hockman, H., Sheridan, W., & Morstyn, G. (1989) · Blood · doi:10.1182/blood.v74.4.1303.1303 · Cited by 137 · cited 1× · see citing works
“A similar hypothesis was offered previously to explain the stability of steady-state neutrophil pools (40).”
Background"Emergency" granulopoiesis in G-CSF-deficient mice in response to Candida albicans infection.
Basu, S., Hodgson, G., Zhang, H.-H., Katz, M., Quilici, C., & Dunn, A. R. (2000) · Blood · doi:10.1182/blood.v95.12.3725.012k06_3725_3733 · Cited by 129 · cited 6×
“However, these cytokines are dispensable for robust granulopoietic responses to inflammation (5, 20).”
BackgroundMethodInfluentialWalker, F., Zhang, H.-H., Matthews, V., Weinstock, J., Nice, E., Ernst, M., Rose-John, S., & Burgess, A. (2008) · Blood · doi:10.1182/blood-2007-10-119636 · Cited by 108 · cited 2× · see citing works
“IL-1 induces the production of many growth factors and inflammatory mediators (33); among these, IL-3, IL-6, G-CSF, and GMCSF have been implicated as agents of emergency granulopoiesis (6, 12).”
BackgroundNeutropenia in high-risk neonates.
Engle, W. D., & Rosenfeld, C. R. (1984) · Jornal de Pediatria · doi:10.1016/s0022-3476(84)80095-5 · Cited by 106 · cited 1× · see citing works
“N eutrophils are vital to innate immunity (1, 2).”
BackgroundYoung, J., Bruno, E., Luens, K., Wu, S., Backer, M., & Murray, L. J. (1996) · Blood · doi:10.1182/blood.v88.5.1619.1619 · Cited by 102 · see citing works
In vivo effects of recombinant interleukin-11 on myelopoiesis in mice.
Hangoc, G., Yin, T., Cooper, S., Schendel, P., Yang, Y. C., & Broxmeyer, H. (1993) · Blood · doi:10.1182/blood.v81.4.965.bloodjournal814965 · Cited by 99 · cited 1×
“2), IL-1RI signals may act through intermediate hematopoietic factors that induce proliferation by both HSC and committed progenitors, such as IL-11 (37, 38) or thrombopoietin (39).”
BackgroundChen, Z., Koralov, S. B., Gendelman, M., Carroll, M., & Kelsoe, G. (2000) · Journal of Immunology · doi:10.4049/jimmunol.164.9.4522 · Cited by 95 · see citing works
Self-citationThe Lineage−c‐Kit+Sca‐1+ Cell Response to Escherichia coli Bacteremia in Balb/c Mice
Zhang, P., Nelson, S., Bagby, G., Siggins, R., Shellito, J., & Welsh, D. A. (2008) · Stem Cells · doi:10.1634/stemcells.2007-1027 · Cited by 94 · cited 1× · see citing works
“IFN- and TNF- can induce Sca-1 expression by lineage-committed progenitors, causing them to mimic the LSK phenotype (31).”
BackgroundIn vivo effects of recombinant interleukin-11 on myelopoiesis in mice
Hangoc, G., Yin, T., Cooper, S. H., Schendel, P. F., Yang, Y., & Broxmeyer, H. (1993) · Blood · doi:10.1182/blood.v81.4.965.965 · Cited by 92 · see citing works
Young, J., Bruno, E., Luens, K., Wu, S., Backer, M., & Murray, L. J. (1996) · Blood · doi:10.1182/blood.v88.5.1619.bloodjournal8851619 · Cited by 84 · cited 1×
“2), IL-1RI signals may act through intermediate hematopoietic factors that induce proliferation by both HSC and committed progenitors, such as IL-11 (37, 38) or thrombopoietin (39).”
BackgroundKoike, K., Stanley, E. R., Ihle, J. N., & Ogawa, M. (1986) · Blood · doi:10.1182/blood.v67.4.859.859 · Cited by 80 · see citing works
Koike, K., Stanley, E., Ihle, J., & Ogawa, M. (1986) · Blood · doi:10.1182/blood.v67.4.859.bloodjournal674859 · Cited by 78 · see citing works
Hibbs, M. L., Quilici, C., Kountouri, N., Seymour, J. F., Armes, J. E., Burgess, A. W., & Dunn, A. R. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.178.10.6435 · Cited by 74 · see citing works
Lemoli, R. M., Fogli, M., Fortuna, A., Motta, M. R., Rizzi, S., Benini, C., & Tura, S. (1993) · PubMed · Cited by 57 · see citing works
Neonatal Neutropenia in Low Birthweight Premature Infants
Gessler, P., Lüders, R., König, S., Haas, N., Lasch, P., & Kachel, W. (1995) · American Journal of Perinatology · doi:10.1055/s-2007-994396 · Cited by 52 · cited 1× · see citing works
“N eutrophils are vital to innate immunity (1, 2).”
BackgroundDividing cells in bone marrow and spleen incorporate bromodeoxyuridine with high efficiency
Schittek, B., Rajewsky, K., & Förster, I. (1991) · European Journal of Immunology · doi:10.1002/eji.1830210136 · Cited by 38 · cited 1× · see citing works
“with BrdU 6 h before sacrifice and compared the frequencies of BrdU cells in each cell compartment from naive and immunized mice (30).”
BackgroundMakinodan, T., Gengozian, N., & Congdon, C. C. (1956) · Journal of Immunology · doi:10.4049/jimmunol.77.4.250 · Cited by 33 · cited 1× · see citing works
“1)F1 mice were sublethally irradiated (600 rad) (26) and reconstituted with equal numbers (5 10(6)) of congenic C57BL/6.”
The phagocytic system in host defense.
Quie, P. G. (1980) · PubMed · Cited by 9 · see citing works
In vitro cloning of hemopoietic cells.
Metcalf, D. (1978) · PubMed · Cited by 3 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Neutrophils in cancer: Neutral no more
Coffelt, S. B., Wellenstein, M. D., & de Visser, K. E. (2016) · Nature reviews. Cancer · doi:10.1038/nrc.2016.52 · Cited by 1,830 · see citing works
Neutrophil: A Cell with Many Roles in Inflammation or Several Cell Types?
Rosales, C. (2018) · Frontiers in Physiology · doi:10.3389/fphys.2018.00113 · Cited by 1,334 · see citing works
“inflammation, IL-1 can also stimulate neutrophil production through the IL-17-G-CSF axis (Ueda et al., 2009), and neutrophils themselves create a positive loop for neutrophil recruitment.”
BackgroundGalli, S. J., Borregaard, N., & Wynn, T. A. (2011) · Nature Immunology · doi:10.1038/ni.2109 · Cited by 1,055 · see citing works
Manz, M. G., & Boettcher, S. (2014) · Nature Reviews Immunology · doi:10.1038/nri3660 · Cited by 855 · see citing works
Immunosuppression mediated by myeloid-derived suppressor cells (MDSCs) during tumour progression
Groth, C., Hu, X., Weber, R., Fleming, V., Altevogt, P., Utikal, J. S., & Umansky, V. (2018) · British Journal of Cancer · doi:10.1038/s41416-018-0333-1 · Cited by 846 · see citing works
Pietras, E. M., Mirantes-Barbeito, C., Fong, S., Loeffler, D., Kovtonyuk, L. V., Zhang, S., Lakshminarasimhan, R., Chin, C. P., Techner, J.-M., Will, B., et al. (2016) · Nature Cell Biology · doi:10.1038/ncb3346 · Cited by 689 · see citing works
Inflammatory modulation of HSCs: viewing the HSC as a foundation for the immune response
King, K. Y., & Goodell, M. A. (2011) · Nature reviews. Immunology · doi:10.1038/nri3062 · Cited by 565 · see citing works
Adipose Tissue Macrophages Promote Myelopoiesis and Monocytosis in Obesity
Nagareddy, P. R., Kraakman, M. J., Masters, S. L., Stirzaker, R. A., Gorman, D. J., Grant, R. W., Dragoljevic, D., Hong, E. S., Abdel‐Latif, A., Smyth, S. S., et al. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.03.029 · Cited by 510 · see citing works
“…certainly plays an important role in inducing myeloid progenitor cell proliferation in response to inflammation, to produce neutrophils and monocytes (Hsu et al., 2011; Ueda et al., 2009), and triggers progenitor cell proliferation via a number of mechanisms in different diseases (Dinarello, 1996).”
BackgroundZhu, G., Zhang, T., Chen, M., Yao, K., Huang, X., Zhang, B., Li, Y., Liu, J., Wang, Y., & Zhao, Z. (2021) · Bioactive Materials · doi:10.1016/j.bioactmat.2021.03.043 · Cited by 501 · see citing works
Demand-adapted regulation of early hematopoiesis in infection and inflammation
Takizawa, H., Boettcher, S., & Manz, M. G. (2012) · Blood · doi:10.1182/blood-2011-12-380113 · Cited by 404 · see citing works
Neutrophil Extracellular Traps: The Biology of Chromatin Externalization
Sollberger, G., Tilley, D. O., & Zychlinsky, A. (2018) · Developmental Cell · doi:10.1016/j.devcel.2018.01.019 · Cited by 346 · see citing works
A Paradoxical Role for Myeloid-Derived Suppressor Cells in Sepsis and Trauma
Cuenca, A. G., Delano, M. J., Kelly‐Scumpia, K. M., Moreno, C. R. D. C., Scumpia, P. O., LaFace, D., Heyworth, P. G., Efron, P. A., & Moldawer, L. L. (2010) · Molecular Medicine · doi:10.2119/molmed.2010.00178 · Cited by 340 · see citing works
“Normally, physiologic numbers of mature neutrophils and monocytes are maintained by a steady-state myelopoietic pathway, whereas either acute infection or an endogenous inflammatory process triggers the mobilization of mature neutrophils and more immature populations from the bone marrow and blood to inflammatory site…”
BackgroundAlum adjuvant: some of the tricks of the oldest adjuvant
Kool, M., Fierens, K., & Lambrecht, B. N. (2011) · Journal of Medical Microbiology · doi:10.1099/jmm.0.038943-0 · Cited by 321 · see citing works
Caiado, F., Pietras, E. M., & Manz, M. G. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20201541 · Cited by 289 · see citing works
Regulation of Inflammation- and Infection-Driven Hematopoiesis
Boettcher, S., & Manz, M. G. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.01.004 · Cited by 265 · see citing works
“The vaccine adjuvant alum, which is a known inducer of IL-1b secretion by stimulating the NLRP3 inflammasome [62], stimulates a hematopoietic response in an IL-1 receptor 1-dependent manner that phenocopies LPS-induced emergency granulopoiesis [63].”
BackgroundTargeting Interleukin-1β Reduces Leukocyte Production After Acute Myocardial Infarction
Sager, H. B., Heidt, T., Hulsmans, M., Dutta, P., Courties, G., Sebas, M., Wojtkiewicz, G. R., Tricot, B., Iwamoto, Y., Sun, Y., et al. (2015) · Circulation · doi:10.1161/circulationaha.115.016160 · Cited by 250 · see citing works
“Increased bone marrow progenitor proliferation after injection of the chemical compound alum, which is used as a vaccination adjuvant, was attenuated in IL-1 receptor–deficient mice.(10) IL-1β also stimulates myelopoiesis in obesity.”
BackgroundInflammasomes in Alveolar Bone Loss
Li, Y., Ling, J., & Jiang, Q. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.691013 · Cited by 215 · see citing works
Interferon-γ impairs proliferation of hematopoietic stem cells in mice
de Bruin, A. M., Demirel, Ö., Hooibrink, B., Brandts, C., & Nolte, M. A. (2013) · Blood · doi:10.1182/blood-2012-05-432906 · Cited by 211 · see citing works
The adaptor molecule CARD9 is essential for tuberculosis control
Dorhoi, A., Desel, C., Yeremeev, V., Pradl, L., Brinkmann, V., Mollenkopf, H., Hanke, K., Groß, O., Ruland, J., & Kaufmann, S. H. E. (2010) · The Journal of Experimental Medicine · doi:10.1084/jem.20090067 · Cited by 202 · see citing works
“Recent studies revealed that granulopoietic emergency program depends on IL-1R signaling and that low IL-1 levels could induce late neutrophilic responses (Ueda et al., 2009).”
BackgroundGriseri, T., McKenzie, B. S., Schiering, C., & Powrie, F. M. (2012) · Immunity · doi:10.1016/j.immuni.2012.08.025 · Cited by 197 · see citing works
“HSCs express receptors for IFNs, IL-1, and IL-6 (Chen et al., 2010; Ueda et al., 2009) and are therefore poised to respond promptly to various inflammatory stimuli.”
BackgroundAlternative Pathways of IL-1 Activation, and Its Role in Health and Disease
Pyrillou, K., Burzynski, L. C., & Clarke, M. C. H. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.613170 · Cited by 188 · see citing works
“More generally, infection and inflammation trigger neutrophilia via IL1-induced proliferation of hematopoietic stem cells, a process known as emergency granulopoiesis (46).”
BackgroundAging drives <i>Tet2</i> <i>+/−</i> clonal hematopoiesis via IL-1 signaling
Caiado, F., Kovtonyuk, L. V., Gonullu, N. G., Fullin, J., Boettcher, S., & Manz, M. G. (2023) · Blood · doi:10.1182/blood.2022016835 · Cited by 161 · see citing works
Cutting Edge: LPS-Induced Emergency Myelopoiesis Depends on TLR4-Expressing Nonhematopoietic Cells
Boettcher, S., Ziegler, P., Schmid, M., Takizawa, H., van Rooijen, N., Köpf, M., Heikenwälder, M. F., & Manz, M. G. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1103253 · Cited by 147 · see citing works
Enhancement of hematopoiesis and lymphopoiesis in diet-induced obese mice
Trottier, M., Naaz, A., Li, Y., & Fraker, P. J. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1205129109 · Cited by 142 · see citing works
Belyaev, N. N., Brown, D. E., Diaz, A. I. G., Rae, A. J., Jarra, W., Thompson, J., Langhorne, J., & Potocnik, A. J. (2010) · Nature Immunology · doi:10.1038/ni.1869 · Cited by 135 · see citing works
Targeting granulocyte apoptosis: mechanisms, models, and therapies
Duffin, R., Leitch, A. E., Fox, S., Haslett, C., & Rossi, A. G. (2010) · Immunological Reviews · doi:10.1111/j.1600-065x.2010.00922.x · Cited by 123 · see citing works
“This may vary under inflammatory conditions where there is knockout animal evidence that IL-1 and tumor necrosis factor-a (TNF-a) can promote a reactive neutrophilia by indirect effects on myeloid progenitors in the absence of other differentiation factors (12).”
BackgroundKwak, H. J., Liu, P., Bajrami, B., Xu, Y., Park, S., Nombela‐Arrieta, C., Mondal, S., Sun, Y., Zhu, H., Chai, L., et al. (2015) · Immunity · doi:10.1016/j.immuni.2014.12.017 · Cited by 116 · see citing works
“In contrast, emergency granulopoiesis is mainly controlled by C/EBPbeta (Hirai et al., 2006; Ueda et al., 2009).”
BackgroundMacNamara, K. C., Oduro, K. A., Martin, O., Jones, D. D., McLaughlin, M., Choi, K., Borjesson, D. L., & Winslow, G. M. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1001893 · Cited by 122 · see citing works
IL-1β-driven neutrophilia preserves antibacterial defense in the absence of the kinase IKKβ
Hsu, L.-C., Enzler, T., Seita, J., Timmer, A. M., Lee, C., Lai, T., Yu, G., Lai, L., Temkin, V., Sinzig, U., et al. (2010) · Nature Immunology · doi:10.1038/ni.1976 · Cited by 119 · see citing works
Inflammatory signaling regulates hematopoietic stem and progenitor cell development and homeostasis
Collins, A., Mitchell, C. A., & Passegué, E. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20201545 · Cited by 111 · see citing works
“Interleukins such as IL-1 and IL-3 have also been implicated in HSC maturation downstream of Runx1.”
BackgroundInfluentialDisordered haematopoiesis and athero-thrombosis
Murphy, A. J., & Tall, A. R. (2016) · European Heart Journal · doi:10.1093/eurheartj/ehv718 · Cited by 109 · see citing works
Seijkens, T. T. P., Hoeksema, M. A., Beckers, L., Smeets, E., Meiler, S. U., Levels, J. H. M., Tjwa, M., de Winther, M. P. J., & Lutgens, E. (2014) · The FASEB Journal · doi:10.1096/fj.13-243105 · Cited by 111 · see citing works
Neutrophils in Tuberculosis: Heterogeneity Shapes the Way?
Lyadova, I. V. (2017) · Mediators of Inflammation · doi:10.1155/2017/8619307 · Cited by 102 · see citing works
“Particularly, CXCL1, CXCL2, CXCL5, TNF-α, and G/GM-CSF stimulate neutrophil migration; TNF-α and IFN-γ activate neutrophils for cytokine/ chemokine production; and IL-1β, G/GM-CSF, and IL-3 prolong neutrophil survival and are involved in granulopoiesis [19, 20, 61, 96].”
BackgroundThe Nlrp3 inflammasome as a “rising star” in studies of normal and malignant hematopoiesis
Ratajczak, M. Z., Bujko, K., Cymer, M., Thapa, A., Adamiak, M., Ratajczak, J., Abdel-Latif, A. K., & Kucia, M. (2020) · Leukemia · doi:10.1038/s41375-020-0827-8 · Cited by 102 · see citing works
Immune cells as tumor drug delivery vehicles
Combes, F., Meyer, E., & Sanders, N. N. (2020) · Journal of Controlled Release · doi:10.1016/j.jconrel.2020.07.043 · Cited by 98 · see citing works
“Nevertheless, the rapid recruitment of endogenous neutrophils in acute inflammatory contexts suggests that some level of short-term trafficking of specific immune cell subsets is possible but we should bear in mind the high number of circulating neutrophils in steady-state conditions [337] and the induced reactive neu…”
BackgroundInhibition of B Lymphopoiesis by Adipocytes and IL-1–Producing Myeloid-Derived Suppressor Cells
Kennedy, D. E., & Knight, K. L. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1500957 · Cited by 97 · see citing works
“The cytokines assessed in conditioned media were IL-1a, IL-1b, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12(p40), IL-12(p70), IL-13, IL-17A, G-CSF, GM-CSF, IFN-g, KC, MCP, MIP-1a, MIP-1b, RANTES, eotaxin, and TNF-a.”
BackgroundInfluentialInflammation triggers emergency granulopoiesis through a density-dependent feedback mechanism
Cain, D. W., Snowden, P. B., Sempowski, G. D., & Kelsoe, G. (2011) · PLoS ONE · doi:10.1371/journal.pone.0019957 · Cited by 95 · see citing works
Self-citationPU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress
Chavez, J. S., Rabe, J. L., Loeffler, D., Higa, K. C., Hernandez, G., Mills, T. S., Ahmed, N., Gessner, R. L., Ke, Z., Idler, B. M., et al. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20201169 · Cited by 91 · see citing works
Regulation of emergency granulopoiesis during infection
Paudel, S., Ghimire, L., Jin, L., Jeansonne, D. P., & Jeyaseelan, S. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.961601 · Cited by 85 · see citing works
“Mice deficient in IL-1R (Il-1r) have reduced proliferation of HSCs, MPPs, and GMP during alum-induced inflammatory granulopoiesis (91).”
BackgroundPutnam, N. E., Fulbright, L. E., Curry, J. M., Ford, C. A., Petronglo, J. R., Hendrix, A. S., & Cassat, J. E. (2019) · PLoS Pathogens · doi:10.1371/journal.ppat.1007744 · Cited by 86 · see citing works
Satake, S., Hirai, H., Hayashi, Y., Shime, N., Tamura, A., Yao, H., Yoshioka, S., Miura, Y., Inaba, T., Fujita, N., et al. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1103007 · Cited by 83 · see citing works
“1C) was enriched in CD11bLy-6G(2)7/4SSC eosinophilic granulocytes (eosinophils (9); Supplemental Fig.”
BackgroundLiu, X., Boyer, M. A., Holmgren, A. M., & Shin, S. (2020) · Cell Host & Microbe · doi:10.1016/j.chom.2020.07.019 · Cited by 78 · see citing works
Normal Hematopoiesis Is a Balancing Act of Self-Renewal and RegenerationPreprint
Olson, O. C., Kang, Y.-A., & Passegue, E. A. (2020) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a035519 · Cited by 78 · see citing works
Hematopoietic responses to SARS-CoV-2 infection
Elahi, S. (2022) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-022-04220-6 · Cited by 79 · see citing works
“Recent evidence suggests that IL-1β promotes cell division and myeloid differentiation of HSCs [71] and is required for stress granulopoiesis [72].”
BackgroundChou, D. B., Sworder, B. J., Bouladoux, N. J., Roy, C. N., Uchida, A. M., Grigg, M. E., Robey, P. G., & Belkaid, Y. (2012) · Journal of Leukocyte Biology · doi:10.1189/jlb.1011527 · Cited by 71 · see citing works
“This myeloerythroid shift occurs in multiple models of inflammation, from bacterial infection to sterile immunization [1–4], and is one pathway that leads to the common condition of anemia in the setting of inflammation.”
BackgroundDisparate adjuvant properties among three formulations of “alum”
Cain, D. W., Sanders, S. E., Cunningham, M. M., & Kelsoe, G. H. (2012) · Vaccine · doi:10.1016/j.vaccine.2012.11.044 · Cited by 69 · see citing works
“Remarkably, the mechanism(s) of alum's adjuvant properties are enigmatic [34], but it is now thought that alum-induced inflammation promotes adaptive immunity [11, 13, 14, 23, 30, 35, 36].”
BackgroundSelf-citationIL-1α Modulates Neutrophil Recruitment in Chronic Inflammation Induced by Hydrocarbon Oil
Lee, P. Y., Kumagai, Y., Xu, Y., Li, Y., Barker, T. T., Liu, C., Sobel, E. S., Takeuchi, O., Akira, S., Satoh, M., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1001328 · Cited by 64 · see citing works
“Indeed, the proliferation of not only neutrophil/ macrophage progenitors, but also multipotent progenitors and hematopoietic stem cells, is supported by IL-1R signaling (44).”
BackgroundOduro, K. A., Liu, F., Tan, Q., Kim, C. K., Lubman, O., Fremont, D. H., Mills, J. C., & Choi, K. (2012) · Blood · doi:10.1182/blood-2011-11-391342 · Cited by 65 · see citing works
Fanti, A.-K., Busch, K., Greco, A., Wang, X., Cirovic, B., Shang, F., Nizharadze, T., Frank, L., Barile, M., Feyerabend, T. B., et al. (2023) · Cell stem cell · doi:10.1016/j.stem.2022.12.014 · Cited by 60 · see citing works
Angiotensin‐converting enzyme is required for normal myelopoiesis
Lin, C. X., Datta, V., Okwan-Duodu, D. K., Chen, X., Fuchs, S., Alsabeh, R., Billet, S., Bernstein, K. E., & Shen, X. Z. (2010) · The FASEB Journal · doi:10.1096/fj.10-169433 · Cited by 63 · see citing works
“Thus, most TPMs are freshly derived from BM. TPMs were stimulated ex vivo, and we then measured the levels of the secreted proinflammatory cytokines TNF- and IL-12/p40 (Fig.”
BackgroundInfluentialJahandideh, B., Derakhshani, M., Abbaszadeh, H., Movassaghpour, A. A., Mehdizadeh, A., Talebi, M., & Yousefi, M. (2020) · Human Immunology · doi:10.1016/j.humimm.2020.01.004 · Cited by 61 · see citing works
Malengier‐Devlies, B., Metzemaekers, M., Wouters, C. H., Proost, P., & Matthys, P. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.766620 · Cited by 62 · see citing works
Barman, P., Urao, N., & Koh, T. (2019) · Journal of Pathology · doi:10.1002/path.5330 · Cited by 50 · see citing works
“However, this process appears to be altered during emergency need of myeloid cells, as in the case of injury or from inflammatory stimuli [33,34].”
BackgroundMacrophages Orchestrate Hematopoietic Programs and Regulate HSC Function During Inflammatory Stress
Seyfried, A. N., Maloney, J., & MacNamara, K. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.01499 · Cited by 44 · see citing works
“The role of nonhematopoietic cells in driving emergency myelopoiesis was illustrated by elegant experiments wherein IL-1R responsiveness was restricted to radio-resistant host cells (129).”
BackgroundDysregulated myelopoiesis and hematopoietic function following acute physiologic insult
Loftus, T. J., Mohr, A. M., & Moldawer, L. L. (2017) · Current Opinion in Hematology · doi:10.1097/moh.0000000000000395 · Cited by 58 · see citing works
Melanoma induced immunosuppression is mediated by hematopoietic dysregulation
Kamran, N., Li, Y., Sierra, M., Alghamri, M. S., Kadiyala, P., Appelman, H. D., Edwards, M. B., Lowenstein, P. R., & Castro, M. G. (2017) · OncoImmunology · doi:10.1080/2162402x.2017.1408750 · Cited by 59 · see citing works
“Cytokines such as G-CSF, GM-CSF and IL-6 have been shown to promote proliferation of granulocytic progenitors in response to infection and chronic inflammation.(19,20)”
BackgroundInterrelation of adipose tissue macrophages and fibrosis in obesity
Dahdah, N., Tercero‐Alcázar, C., Malagón, M. M., García-Rovés, P. M., & Guzmán‐Ruiz, R. (2024) · Biochemical Pharmacology · doi:10.1016/j.bcp.2024.116324 · Cited by 61 · see citing works
Prigge, J. R., Hoyt, T., Dobrinen, E., Capecchi, M. R., Schmidt, E. E., & Meissner, N. N. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1501553 · Cited by 57 · see citing works
Higa, K. C., Goodspeed, A., Chavez, J. S., De Dominici, M., Danis, E., Zaberezhnyy, V., Rabe, J. L., Tenen, D. G., Pietras, E. M., & DeGregori, J. (2021) · Journal of Experimental Medicine · doi:10.1084/jem.20200560 · Cited by 57 · see citing works
“Chronic IL-1β–induced Cebpa-knockout MPP3 expansion is cell cycle independent IL-1β can stimulate HSPC proliferation (Pietras et al., 2016; Ueda et al., 2009; Weisser et al., 2016).”
BackgroundInflammation Regulates Haematopoietic Stem Cells and Their Niche
Ho, N. P. Y., & Takizawa, H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23031125 · Cited by 48 · see citing works
Eislmayr, K., Bestehorn, A., Morelli, L., Borroni, M., Walle, L. V., Lamkanfi, M., & Kovarik, P. (2022) · Science Advances · doi:10.1126/sciadv.abj7293 · Cited by 47 · see citing works
“Nevertheless, IL-1 is not likely to directly stimulate granulopoiesis in vivo since Il1r1-dependent reactive neutrophilia requires the expression of Il1r1 on radiation-resistant but not hematopoietic cells (29).”
BackgroundInfluentialmicroRNAs as potential regulators of myeloid-derived suppressor cell expansion
El-Gazzar, M. M. (2013) · Innate Immunity · doi:10.1177/1753425913489850 · Cited by 44 · see citing works
“Under physiological stress, such as in response to infection or a growing tumor, there is a need for expansion of the myeloid cell pool in the bone marrow and spleen to compensate for the loss of innate immune cells during inflammatory processes.(30,31) This prompted the proposal that immature myeloid progenitors (i.”
BackgroundMaintenance of high-turnover tissues during and beyond homeostasis
Banjac, I., Maimets, M., & Jensen, K. B. (2023) · Cell stem cell · doi:10.1016/j.stem.2023.03.008 · Cited by 37 · see citing works
IL-1 in aging and pathologies of hematopoietic stem cells
Caiado, F., & Manz, M. G. (2024) · Blood · doi:10.1182/blood.2023023105 · Cited by 38 · see citing works
The Role of the Bone Marrow Microenvironment in the Response to Infection
Johnson, C. B., Zhang, J., & Lucas, D. (2020) · Frontiers in Immunology · doi:10.3389/fimmu.2020.585402 · Cited by 35 · see citing works
“org 2 that in response to the adjuvant alum, the BM initiated IL1 mediated emergency granulopoiesis (32).”
BackgroundNeutrophil homeostasis and its regulation by danger signaling
Wirths, S., Bugl, S., & Kopp, H. (2014) · Blood · doi:10.1182/blood-2013-11-516260 · Cited by 34 · see citing works
Zhu, H., Kwak, H. J., Liu, P., Bajrami, B., Xu, Y., Park, S., Nombela‐Arrieta, C., Mondal, S., Kambara, H., Yu, H., et al. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1602006 · Cited by 32 · see citing works
“For instance, steady-state granulopoiesis is regulated by the C/EBP-a, but not the /EBP-b, transcription factor (7, 8).”
BackgroundInfluentialIncreased Fanconi C expression contributes to the emergency granulopoiesis response
Hu, L., Huang, W., Hjort, E. E., & Eklund, E. A. (2013) · Journal of Clinical Investigation · doi:10.1172/jci69032 · Cited by 33 · see citing works
Herrera, M., Salva, S., Villena, J., Barbieri, N., Marranzino, G., & Alvarez, S. (2014) · PLoS ONE · doi:10.1371/journal.pone.0090227 · Cited by 28 · see citing works
Kaplan, I. M., Morisot, S., Heiser, D., Cheng, W., Kim, M. J., & Civin, C. I. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1002806 · Cited by 26 · see citing works
“This phenotype strongly resembles reactive granulopoiesis (2, 4, 6), in which these mature cells of the immune system respond rapidly to immunogenic insults, such as infection or adjuvant treatment.”
BackgroundInfluentialMelvan, J. N., Siggins, R. W., Stanford, W. L., Porretta, C., Nelson, S., Bagby, G. J., & Zhang, P. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1102395 · Cited by 26 · see citing works
“Although inflammatory cytokines, including G-CSF, GM-CSF, IL-1, and IL-6, are well-recognized regulators of granulopoiesis, increasing evidence suggests that pathogens can directly modify marrow hematopoiesis through TLR stimulation of hematopoietic precursors (5, 6, 8, 40, 41).”
BackgroundHoxA10 Terminates Emergency Granulopoiesis by Increasing Expression of Triad1
Wang, H., Bei, L., Shah, C. A., Hu, L., & Eklund, E. A. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1401909 · Cited by 25 · see citing works
Hu, L., Huang, W., Hjort, E. E., Bei, L., Platanias, L. C., & Eklund, E. A. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.681361 · Cited by 23 · see citing works
Reece, P., Baatjes, A. J., Cyr, M. M., Sehmi, R., & Denburg, J. A. (2013) · Immunology · doi:10.1111/imm.12078 · Cited by 21 · see citing works
The Role of Microbiota and Immunobiotics in Granulopoiesis of Immunocompromised Hosts
Salva, S., & Alvarez, S. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00507 · Cited by 20 · see citing works
“Hence, the neutrophilia induced by infection or inflammation is assisted by both GM-CSF and IL-1, which in turn accelerates granulopoiesis by expanding MPP and CMP compartments (38).”
BackgroundThe bone marrow hematopoietic niche and its adaptation to infection
Gomes, A. C., Saraiva, M., & Gomes, M. S. (2021) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2020.05.014 · Cited by 18 · see citing works
Nfia deletion in myeloid cells blocks expansion of myeloid-derived suppressor cells during sepsis
Dai, J., Kumbhare, A., Williams, D. A., Youssef, D. A., Yao, Z. Q., McCall, C. E., & Gazzar, M. E. (2017) · Innate Immunity · doi:10.1177/1753425917742956 · Cited by 19 · see citing works
Salva, S., Kolling, Y., Ivir, M., Gutiérrez, F., & Alvarez, S. (2021) · Frontiers in Nutrition · doi:10.3389/fnut.2021.704868 · Cited by 20 · see citing works
“At the same time, the lack of increase in GMCSF and IL-1 in bone marrow is responsible for a defective emergency granulopoiesis against the infectious challenge by not expanding the multipotent progenitors and common lymphoid and myeloid progenitors (29, 43, 44).”
BackgroundATF3 Reprograms the Bone Marrow Niche in Response to Early Breast Cancer Transformation
Perrone, M., Chiodoni, C., Lecchi, M., Botti, L., Bassani, B., Piva, A., Jachetti, E., Milani, M., Lecis, D., Tagliabue, E., et al. (2022) · Cancer Research · doi:10.1158/0008-5472.can-22-0651 · Cited by 17 · see citing works
Falahee, P. C., Anderson, L., Reynolds, M. B., Pirir, M., McLaughlin, B. E., Dillen, C. A., Cheung, A. L., Miller, L. S., & Simon, S. I. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1700649 · Cited by 17 · see citing works
Type I interferons drive inflammasome-independent emergency monocytopoiesis during endotoxemia
Lasseaux, C., Fourmaux, M.-P., Chamaillard, M., & Poulin, L. F. (2017) · Scientific Reports · doi:10.1038/s41598-017-16869-2 · Cited by 17 · see citing works
HogenEsch, H., Dunham, A. D., Burlet, E., Lu, F., Mosley, Y. C., & Morefield, G. L. (2016) · Journal of Applied Toxicology · doi:10.1002/jat.3349 · Cited by 16 · see citing works
“A single intraperitoneal injection of a large dose of alum-precipitated protein induced neutrophilia in an IL-1RI and granulocyte colony-stimulating factor-dependent manner suggesting that the mobilization of neutrophils is regulated by IL-1 and granulocyte colony-stimulating factor (Cain et al., 2011; Ueda et al., 20…”
BackgroundBarman, P., Pang, J., Urao, N., & Koh, T. (2019) · Journal of Immunology · doi:10.4049/jimmunol.1801481 · Cited by 14 · see citing works
“Expansion of HSPC and MPP populations was observed following alum administration in mice (15); our MPP3 population would be found in the HSPC population of this previous study based on the markers used.”
BackgroundResultInfluentialChavez, J. S., Rabe, J. L., Hernandez, G., Mills, T., Niño, K. E., Davizon‐Castillo, P., & Pietras, E. M. (2022) · Cells · doi:10.3390/cells11040680 · Cited by 15 · see citing works
“IL-1β induces numerous changes in the blood system, including increased production of myeloid cells and platelets to facilitate host defense and tissue repair [3,4].”
BackgroundMurray, P. J. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.04.010 · Cited by 15 · see citing works
“IL-1R signaling has previously been shown to control neutrophil production in alum-induced inflammation (Ueda et al., 2009).”
BackgroundInflammation and Immunopathogenesis of Tuberculosis Progression
Lyadova, I. V. (2012) · InTech eBooks · doi:10.5772/32060 · Cited by 15 · see citing works
“In addition, IL-1 is highly chemotactic for T lymphocytes, stimulates CD4+ T cell proliferation and IFN- production, controls early processes of granuloma formation, and stimulates the generation and the recruitment of neutrophils (Hunninghake et al., 1987; Sugawara et al., 2001; Miller et al., 2007; Oliveira et al.…”
BackgroundPU.1 is required to restrain myelopoiesis during chronic inflammatory stress
Chavez, J. S., Rabe, J. L., Niño, K. E., Wells, H. H., Gessner, R. L., Mills, T. S., Hernandez, G., & Pietras, E. M. (2023) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2023.1204160 · Cited by 14 · see citing works
“IL-1β is produced in response to a wide range of physiological insults, and IL-1 signaling is closely linked to a wide variety of chronic inflammatory diseases, where it plays a critical role in the activation of inflammatory myelopoiesis (Ueda et al., 2009; Dinarello, 2011; Mirantes et al., 2014; Pietras, 2017).”
BackgroundLibregts, S. F. W. M., & Nolte, M. A. (2014) · Experimental Cell Research · doi:10.1016/j.yexcr.2014.09.016 · Cited by 14 · see citing works
Cell-Intrinsic In Vivo Requirement for the E47–p21 Pathway in Long-Term Hematopoietic Stem Cells
Santos, P. M. L., Ding, Y., & Borghesi, L. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1302502 · Cited by 14 · see citing works
“In reactive neutrophilia, multipotent HSCs and MPPs, as well as bipotent granulocytemonocyte progenitors, contribute to accelerated granulopoiesis (23, 28, 29).”
BackgroundLiu, G., Liu, Z., Lin, Z., Chen, P., Yan, Y.-C., Lin, Q., Hu, Y., Jiang, N., & Yu, B. (2023) · Stem Cell Research & Therapy · doi:10.1186/s13287-023-03454-w · Cited by 14 · see citing works
“This adaptive response of HSPCs to inflammation can promote the elimination of inflammation [76, 86, 87], indicating that HSPCs play a vital role in the body’s response to inflammation.”
BackgroundThe effect of inflammatory factors and their inhibitors on the hematopoietic stem cells fate
Najafi, S., Ghanavat, M., Shahrabi, S., Gatavizadeh, Z., & Saki, N. (2021) · Cell Biology International · doi:10.1002/cbin.11545 · Cited by 13 · see citing works
“The exact mechanism of IL‐1 function on HSCs is not recognized, but studies show that this cytokine can stimulate myeloid differentiation through PU.1 upre- gulation (Pietras et al., 2016; Ueda et al., 2009).”
BackgroundQian, L., Xiang, D., Zhang, J., Zhu, S., Gao, J., Wang, X., Gao, J., Zhang, Y., Shen, J., Yu, Y., et al. (2012) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2012.11.002 · Cited by 13 · see citing works
Analysis of Murine Hematopoietic Stem Cell Proliferation During Inflammation
Jalbert, E., & Pietras, E. M. (2017) · Methods in molecular biology · doi:10.1007/978-1-4939-7371-2_14 · Cited by 12 · see citing works
Ma, T., Liu, J., Gao, Z., Li, Y., Lin, J., Pang, K., Li, R. Q., Zhang, X., Tang, L., Liu, Y., et al. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03589-y · Cited by 10 · see citing works
“…enhanced proliferation and myeloid differentiation mediated by the adaptor protein MyD88 and various signaling pathways including NF-κB and PU.1; [42–44] (2) IL1R1-deficient ( Il1r1 / ) mice showed markedly reduced BM-derived cells and diminished monopoiesis, indicating the necessity of IL-1…”
Horrigan, O., Jose, S., Mukherjee, A., Sharma, D., Huber, A., & Madan, R. (2021) · Frontiers in Cellular and Infection Microbiology · doi:10.3389/fcimb.2021.619192 · Cited by 10 · see citing works
“A role for non-hematopoietic cells in controlling the generation and mobilization of neutrophils after noxious insults has been previously reported (Ueda et al., 2009; Boettcher et al., 2012; Burberry et al., 2014).”
BackgroundHeme oxygenase 1 affects granulopoiesis in mice through control of myelocyte proliferation
Bukowska-Straková, K., Cieśla, M., Szade, K., Nowak, W. N., Straka, R., Szade, A., Tyszka‐Czochara, M., Najder, K., Konturek-Cieśla, A., Siedlar, M., et al. (2016) · Immunobiology · doi:10.1016/j.imbio.2016.10.018 · Cited by 10 · see citing works
Zebrafish: a convenient tool for myelopoiesis research
Hu, Y.-X., & Jing, Q. (2023) · Cell Regeneration · doi:10.1186/s13619-022-00139-2 · Cited by 10 · see citing works
Shah, C. A., Broglie, L., Hu, L., Bei, L., Huang, W., Dressler, D. B., & Eklund, E. A. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra117.000528 · Cited by 9 · see citing works
Huang, W., Liu, B., & Eklund, E. A. (2020) · Leukemia · doi:10.1038/s41375-020-0771-7 · Cited by 9 · see citing works
Gianni’, M., Fratelli, M., Bolis, M., Kurosaki, M., Zanetti, A., Paroni, G., Rambaldi, A., Borleri, G., Rochette‐Egly, C., Terao, M., et al. (2016) · Oncotarget · doi:10.18632/oncotarget.10556 · Cited by 9 · see citing works
“Steady-state granulopoiesis requires the PU.1 and C-EBPα transcription factors [56–58], while stress granulopoiesis is stimulated by inflammatory cytokines like interferon [42, 43], IL-6, IL-3 and IL-1 [44].”
BackgroundInfluential
- Authors
- Ueda, Y., Cain, D. W., Kuraoka, M., Kondo, M., & Kelsoe, G.
- Affiliations
- Duke Medical Center (US)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2009-05
- Volume
- 182
- Issue
- 10
- Pages
- 6477-6484
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC2780360
- OpenAlex
- W1647595030
- Cited by
- 138
- References
- 49
- Citations by year
- 2026: 6 · 2025: 8 · 2024: 7 · 2023: 7 · 2022: 8 · 2021: 13 · 2020: 13 · 2019: 5 · 2018: 6 · 2017: 11 · 2016: 7 · 2015: 7 · 2014: 7 · 2013: 6 · 2012: 11
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (CA98129, R01CA098129)
- National Institute of Allergy and Infectious Diseases (R01AI056123, AI56123, R01AI024335, AI 24335, U19AI056363, AI-56363)
- Topics
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Blood disorders and treatments
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- IL-1 receptor type I, hematopoietic stem cells, emergency granulopoiesis, CFU-GM, multipotent progenitors, HSC proliferation, inflammation, radiation chimeras, eosinophilia, antibody production
- MeSH terms
- Adjuvants, Immunologic, Alum Compounds, Animals, Cell Differentiation, Flow Cytometry, Granulocytes, Hematopoiesis, Hematopoietic Stem Cells, Inflammation, Interleukin-1, Neutrophils, RNA, Messenger, Polymerase Chain Reaction, Receptors, Interleukin-1, Mice, Knockout, Multipotent Stem Cells, Cell Proliferation, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
