Cited by 646Immune Response and InflammationTuberculosis Research and EpidemiologyImmune cells in cancer

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Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens

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El Kasmi, Karim C, Qualls, Joseph E, Pesce, John T, Smith, Amber M, Thompson, Robert W, Henao-Tamayo, Marcela, Basaraba, Randall J, König, Till, Schleicher, Ulrike, Koo, Mi-Sun, Kaplan, Gilla, Fitzgerald, Katherine A, Tuomanen, Elaine I, Orme, Ian M, Kanneganti, Thirumala-Devi, Bogdan, Christian, Wynn, Thomas A, Murray, Peter J·2008·Nature Immunology

DOI 10.1038/ni.1671PMC PMC2584974

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Abstract

Toll-like receptor (TLR) signaling in macrophages is required for antipathogen responses, including the biosynthesis of nitric oxide from arginine, and is essential for immunity to Mycobacterium tuberculosis, Toxoplasma gondii and other intracellular pathogens. Here we report a 'loophole' in the TLR pathway that is advantageous to these pathogens. Intracellular pathogens induced expression of the arginine hydrolytic enzyme arginase 1 (Arg1) in mouse macrophages through the TLR pathway. In contrast to diseases dominated by T helper type 2 responses in which Arg1 expression is greatly increased by interleukin 4 and 13 signaling through the transcription factor STAT6, TLR-mediated Arg1 induction was independent of the STAT6 pathway. Specific elimination of Arg1 in macrophages favored host survival during T. gondii infection and decreased lung bacterial load during tuberculosis infection.

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Alternative activation of macrophages
Gordon, S. (2003) · Nature Reviews Immunology · doi:10.1038/nri978 · Cited by 6,189 · cited 1×
“Although macrophage Arg1 expression is commonly linked to the hypothesized antiworm functions of alternatively activated macrophages (AAMs”
Background
Nitric oxide and the immune response
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Medzhitov, R. (2007) · Nature · doi:10.1038/nature06246 · Cited by 2,862 · cited 1×
“1671" language="eng" relation="no"> In macrophages, Toll-like receptors (TLRs) activate protective immune responses, including recognition of pathogens, activation of antipathogen effector pathways and transition to protective adaptive response”
Background
Regulation of immune responses by L-arginine metabolism
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“Although macrophage Arg1 expression is commonly linked to the hypothesized antiworm functions of alternatively activated macrophages (AAMs”
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Fibrotic disease and the TH1/TH2 paradigm
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“TLR and interferon pathways synergistically trigger NO production by transcriptional and post-transcriptional mechanisms that enhance expression of inducible nitric oxide synthase (iNOS), the enzyme responsible for NO production from arginine in macrophage”
Background
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Arginase-1 Expression in Myeloid Cells Regulates Staphylococcus aureus Planktonic but Not Biofilm Infection
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Background
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Background
Blocking IL-10 receptor signaling ameliorates Mycobacterium tuberculosis infection during influenza-induced exacerbation
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“Since AAM support the intracellular persistence of Mtb (45, 59) 423”
Background
Metabolic Regulation of Immune Responses to Mycobacterium tuberculosis: A Spotlight on L-Arginine and L-Tryptophan Metabolism
Crowther, R. R., & Qualls, J. E. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2020.628432 · Cited by 36
Self-citation
Microglia in Neurodegenerative Events—An Initiator or a Significant Other?
Harry, G. J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115818 · Cited by 37
“For example, Arg1 is also induced in M1 macrophages [26].”
Background
Inhibition of Nitric Oxide Production in Activated Macrophages Caused by Toxoplasma gondii Infection Occurs by Distinct Mechanisms in Different Mouse Macrophage Cell Lines
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l -Arginine Synthesis from l -Citrulline in Myeloid Cells Drives Host Defense against Mycobacteria In Vivo
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“Arginase 1 (Arg1), which metabolizes L-ARG to urea and L-ornithine (L-ORN), is expressed in macrophages following mycobacterial infection, thus limiting L-ARG–dependent antimycobacterial defenses (7, 8).”
BackgroundSelf-citation
Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities
Llibre, A., Dedicoat, M. J., Burel, J. G., Demangel, C., O’Shea, M. K., & Mauro, C. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.747387 · Cited by 37
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Background
Context‐dependent regulation of Th17‐associated genes and IFNγ expression by the transcription factor NFAT5
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Background
Controlled light-induced gas phase nitric oxide release from S-nitrosothiol-doped silicone rubber films
Lautner, G., Stringer, B. B., Brisbois, E. J., Meyerhoff, M. E., & Schwendeman, S. P. (2019) · Nitric Oxide · doi:10.1016/j.niox.2019.01.016 · Cited by 35
“RSNOs have absorption maxima at wavelengths around 340 nm (1(n,π*)) and 520–590 nm (1(π,π*)), and these wavelengths have been primarily associated with their decomposition [20,21].”
Background
Propolis Exerts an Anti-Inflammatory Effect on PMA-Differentiated THP-1 Cells via Inhibition of Purine Nucleoside Phosphorylase
Alqarni, A. M., Niwasabutra, K., Sahlan, M., Fearnley, H., Fearnley, J., Ferro, V. A., & Watson, D. G. (2019) · Metabolites · doi:10.3390/metabo9040075 · Cited by 35
“The ability to sustain NO generation plays a crucial role in macrophage adaptation that allows for killing of intracellular mycobacteria [77,78].”
Background
Selective Endothelial Overexpression of Arginase II Induces Endothelial Dysfunction and Hypertension and Enhances Atherosclerosis in Mice
Vaisman, B. L., Andrews, K. L., Khong, S. M. L., Wood, K. C., Moore, X. L., Fu, Y., Kepka‐Lenhart, D., Morris, S. M., Remaley, A. T., & Chin-Dusting, J. P. F. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039487 · Cited by 35
“Likely dependent on the site of integration into chromosomal DNA, the Tie2 promoter has, at least in one case, been found to drive expression of a transgene in myeloid cells [37].”
Background
Gene expression profiling in stroke: relevance of blood–brain interaction
Asano, S., Chantler, P. D., & Barr, T. L. (2015) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2015.10.004 · Cited by 34
Integrated analysis of ischemic stroke datasets revealed sex and age difference in anti-stroke targets
Li, W., Dai, S., Wang, Q., Guo, Y., Yi, H., Zheng, J., Liu, J., Liu, D., Li, G., & Huang, J. (2016) · PeerJ · doi:10.7717/peerj.2470 · Cited by 34
Oligodendroglia Are Particularly Vulnerable to Oxidative Damage After Neurotrauma In Vivo
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Tsc1 is a Critical Regulator of Macrophage Survival and Function
Fang, C., Yu, J., Luo, Y., Chen, S., Wang, W., Zhao, C., Sun, Z., Wu, W., Guo, W., Han, Z., et al. (2015) · Cellular Physiology and Biochemistry · doi:10.1159/000430306 · Cited by 33
Myeloid Cell Arg1 Inhibits Control of Arthritogenic Alphavirus Infection by Suppressing Antiviral T Cells
Burrack, K. S., Tan, J. J. L., McCarthy, M. K., Her, Z., Berger, J. N., Ng, L. F. P., & Morrison, T. E. (2015) · PLoS Pathogens · doi:10.1371/journal.ppat.1005191 · Cited by 33
“Indeed, Arg1 activity in myeloid cells impairs effective immunity against intracellular pathogens such asMycobacterium tuberculosis and Toxoplasma gondii [38], exacerbates tumor growth by suppressing T cell function [39,40], and limits T cell-driven inflammatory Myeloid Cell Arg1 Inhibits Antiviral T Cells”
Background
Lethal phenotype in conditional late-onset arginase 1 deficiency in the mouse
Kasten, J., Hu, C., Bhargava, R., Park, H., Tai, D. S., Byrne, J., Marescau, B., Deyn, P. P. D., Schlichting, L., Grody, W. W., et al. (2013) · Molecular Genetics and Metabolism · doi:10.1016/j.ymgme.2013.06.020 · Cited by 33
“To study the pathophysiology of arginase deficiency systematically in an adult animal model of the disease, we induced widespread arginase 1 deficiency in adult animals by using a conditional arginase 1 knockout mouse strain [17].”
Background
SPI-1 encoded genes of Salmonella Typhimurium influence differential polarization of porcine alveolar macrophages in vitro
Kýrová, K., Štěpánová, H., Rychlı́k, I., Faldyna, M., & Volf, J. (2012) · BMC Veterinary Research · doi:10.1186/1746-6148-8-115 · Cited by 33
“This can be explained by the fact that, although these genes are related to M2 [7], IL-10 can be activated by the NF-κB signaling pathway in the late phases of infection to quell the immune response [24] and arginase-1 is induced following toll like receptor stimulation [25].”
Background
Effect of Sema4D on microglial function in middle cerebral artery occlusion mice
Sawano, T., Watanabe, F., Ishiguchi, M., Doe, N., Furuyama, T., & Inagaki, S. (2015) · Glia · doi:10.1002/glia.22890 · Cited by 32
Neutrophils and Close Relatives in the Hypoxic Environment of the Tuberculous Granuloma: New Avenues for Host-Directed Therapies?
Rémot, A., Doz, E., & Winter, N. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00417 · Cited by 30
“(104, 105) and is detected in necrotizing granulomas in”
Background
Genipin guides and sustains the polarization of macrophages to the pro-regenerative M2 subtype via activation of the pSTAT6-PPAR-gamma pathway
Isali, I., McClellan, P. E., Shankar, E., Gupta, S., Jain, M. K., Anderson, J. M., Hijaz, A., & Akkuş, O. (2021) · Acta Biomaterialia · doi:10.1016/j.actbio.2021.06.043 · Cited by 34
Alphavirus-Driven Interferon Gamma (IFNg) Expression Inhibits Tumor Growth in Orthotopic 4T1 Breast Cancer Model
Trofimova, O., Korotkaja, K., Skrastiņa, D., Jansons, J., Spunde, K., Isaguliants, M. G., & Zajakina, A. (2021) · Vaccines · doi:10.3390/vaccines9111247 · Cited by 32
Protein energy malnutrition increases arginase activity in monocytes and macrophages
Corware, K., Yardley, V., Mack, C., Schuster, S., Al-Hassi, H. O., Herath, S., Bergin, P. J., Modolell, M., Munder, M., Müller, I., et al. (2014) · Nutrition & Metabolism · doi:10.1186/1743-7075-11-51 · Cited by 31
“Whereas arginase upregulation in macrophages during PEM is STAT6- or TLRs- dependent remains to be established [57].”
Background
Spatially Targeted Proteomics of the Host–Pathogen Interface during Staphylococcal Abscess Formation
Guiberson, E. R., Weiss, A., Ryan, D. J., Monteith, A. J., Sharman, K., Gutierrez, D. B., Perry, W., Caprioli, R. M., Skaar, E. P., & Spraggins, J. M. (2020) · ACS Infectious Diseases · doi:10.1021/acsinfecdis.0c00647 · Cited by 32
Bone marrow cell derived arginase I is the major source of allergen-induced lung arginase but is not required for airway hyperresponsiveness, remodeling and lung inflammatory responses in mice
Niese, K. A., Collier, A. R., Hajek, A. R., Cederbaum, S. D., O’Brien, W. E., Wills-Karp, M. A., Rothenberg, M. E., & Zimmermann, N. (2009) · BMC Immunology · doi:10.1186/1471-2172-10-33 · Cited by 30
“and Nipostrongylus brasiliensis [11-16] demonstrated a role for arginase expression in host defense.”
Background
C-type lectins with a sweet spot forMycobacterium tuberculosis
Lugo‐Villarino, G., Hudrisier, D., Tanne, A. J., & Neyrolles, O. (2011) · European Journal of Microbiology and Immunology · doi:10.1556/eujmi.1.2011.1.6 · Cited by 32
The flux of energy in critical illness and the obesity paradox
Jaitovich, A., & Hall, J. B. (2025) · Physiological Reviews · doi:10.1152/physrev.00029.2024 · Cited by 34
The immunopathology of lung fibrosis: amphiregulin-producing pathogenic memory T helper-2 cells control the airway fibrotic responses by inducing eosinophils to secrete osteopontin
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RETRACTED ARTICLE: Ornithine-A urea cycle metabolite enhances autophagy and controls Mycobacterium tuberculosis infection
Thandi, R. S., Radhakrishnan, R. K., Tripathi, D., Paidipally, P., Azad, A. K., Schlesinger, L. S., Samten, B., Mulik, S., & Vankayalapati, R. (2020) · Nature Communications · doi:10.1038/s41467-020-17310-5 · Cited by 30
Retracted
Macrophage-Assisted Inflammation and Pharmacological Regulation of the Cholinergic Anti-Inflammatory Pathway
Pohanka, M., Snopková, S., Havlíčková, K., Boštík, P., Šinkorová, Z., Fusek, J., Kuča, K., & Pikula, J. (2011) · Current Medicinal Chemistry · doi:10.2174/092986711794480140 · Cited by 30
“The infections, which induce this shift from Th1 to Th2, include those caused by measles virus, HIV, Schistosoma and Trypanosoma [58, 59].”
Background
Mesenchymal Stem Cells and Myeloid Derived Suppressor Cells: Common Traits in Immune Regulation
Lyadova, I. V., Sosunova, E., Николаев, А. А., & Nenasheva, T. A. (2016) · Journal of Immunology Research · doi:10.1155/2016/7121580 · Cited by 30
“The studies have reported the inhibition of IFN-𝛾 [62] and Th17 [63], and both the stimulation [64, 65] and the suppression [66] of Th2 responses by ARG1 produced by various cells.”
Severe Listeria monocytogenes Infection Induces Development of Monocytes with Distinct Phenotypic and Functional Features
Drevets, D. A., Schawang, J. E., Mandava, V. K., Dillon, M. J., & Leenen, P. J. M. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1000486 · Cited by 29
“However, Arg1 mRNA expression also increased progressively in these cells, suggesting an increasing limitation to use arginine for NO production (27).”
Background
Resolution of Cutaneous Leishmaniasis and Persistence of Leishmania major in the Absence of Arginase 1
Paduch, K., Debus, A., Rai, B., Schleicher, U., & Bogdan, C. (2019) · The Journal of Immunology · doi:10.4049/jimmunol.1801249 · Cited by 29
Self-citation
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Regulated Arginine Metabolism in Immunopathogenesis of a Wide Range of Diseases: Is There a Way to Pass between Scylla and Charybdis?
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IL-4Rα-Dependent Alternative Activation of Macrophages Is Not Decisive for Mycobacterium tuberculosis Pathology and Bacterial Burden in Mice
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“[13, 17] and confirm their findings in vivo using the hypervirulent Beijing strain,MtbHN878 and LysMIL-4Rα mice, which are deficient for IL-4Rα in macrophages and neutrophils [18].”
BackgroundInfluential
The cationic amino acid transporter 2 is induced in inflammatory lung models and regulates lung fibrosis
Niese, K. A., Chiaramonte, M. G., Ellies, L. G., Rothenberg, M. E., & Zimmermann, N. (2010) · Respiratory Research · doi:10.1186/1465-9921-11-87 · Cited by 29
Elevated CD14 (Cluster of Differentiation 14) and Toll‐Like Receptor (TLR) 4 Signaling Deteriorate Periapical Inflammation in TLR2 Deficient Mice
Rider, D. B., Furusho, H., Xu, S., Trachtenberg, A. J., Kuo, W. P., Hirai, K., Susa, M., Bahammam, L. A., Stashenko, P., Fujimura, A., et al. (2016) · The Anatomical Record · doi:10.1002/ar.23383 · Cited by 28
Differential Gene Expression in the EphA4 Knockout Spinal Cord and Analysis of the Inflammatory Response Following Spinal Cord Injury
Munro, K. M., Perreau, V. M., & Turnley, A. M. (2012) · PLoS ONE · doi:10.1371/journal.pone.0037635 · Cited by 27
“pathway following parasitic infection [39,40].”
Efficacy and Effect of Inhaled Adenosine Treatment in Hospitalized COVID-19 Patients
Caracciolo, M., Correale, P., Mangano, C., Foti, G., Falcone, C., Macheda, S., Cuzzola, M., Conte, M., Falzea, A. C., Iuliano, E., et al. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.613070 · Cited by 29
Promotion of Anti-Tuberculosis Macrophage Activity by L-Arginine in the Absence of Nitric Oxide
McKell, M. C., Crowther, R. R., Schmidt, S., Robillard, M. C., Cantrell, R., Lehn, M. A., Janssen, E. M., & Qualls, J. E. (2021) · Frontiers in Immunology · doi:10.3389/fimmu.2021.653571 · Cited by 27
“Furthermore, mycobacteria-mediated upregulation of the L-arginine consuming enzyme – arginase 1 (Arg1) – in macrophages decreases host defenses against this pathogen (45, 46).”
BackgroundSelf-citation
Substrate-mediated regulation of the arginine transporter of Toxoplasma gondii
Rajendran, E., Clark, M., Goulart, C., Steinhöfel, B., Tjhin, E. T., Gross, S., Smith, N. C., Kirk, K., & van Dooren, G. G. (2021) · PLoS Pathogens · doi:10.1371/journal.ppat.1009816 · Cited by 24
An Epidermal-Specific Role for Arginase1 during Cutaneous Wound Repair
Crompton, R. A., Williams, H., Campbell, L., Lim, H. K., Saville, C. R., Ansell, D. M., Reid, A. J., Wong, J. K. F., Vardy, L. A., Hardman, M. J., et al. (2021) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2021.09.009 · Cited by 28
Co-existence of classical and alternative activation programs in macrophages responding to Toxoplasma gondii
Patil, V., Zhao, Y., Shah, S. M., Fox, B. A., Rommereim, L. M., Bzik, D. J., & Yap, G. S. (2013) · International Journal for Parasitology · doi:10.1016/j.ijpara.2013.08.003 · Cited by 27
“…in vivo, we investigated the expression of M1 and M2 markers in macrophages responding to T. gondii infection, where induction of the M2-associated arginase-1 (Arg1) has been reported (El Kasmi et al., 2008), against the backdrop of a classical Th1-dominated immune response (Yap et al., 2006).”
Background
S-Nitrosation of arginase 1 requires direct interaction with inducible nitric oxide synthase
Dunn, J., Gutbrod, S. R., Webb, A. K., Pak, A., Jandu, S. K., Bhunia, A. K., Berkowitz, D. E., & Santhanam, L. (2011) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-011-0841-2 · Cited by 27
“Furthermore, mice deficient in macrophage Arg1 have higher NO in tissues associated with Mycobacterium tuberculosis infection and improved host control of the organism as measured by granuloma size [29].”
Arc of a Vicious Circle
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High mortality of juvenile gilthead sea bream (Sparus aurata) from photobacteriosis is associated with alternative macrophage activation and anti-inflammatory response: Results of gene expression profiling of early responses in the head kidney
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Hematopoietic arginase 1 deficiency results in decreased leukocytosis and increased foam cell formation but does not affect atherosclerosis
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Background
Innate immunity in sarcoidosis pathobiology
Chen, E. S. (2016) · Current Opinion in Pulmonary Medicine · doi:10.1097/mcp.0000000000000305 · Cited by 25
“tuberculosis remains unknown, but these phenotypes bear attenuated antimicrobial capabilities through the induction of type-1 arginase, which inhibits iNOS function [49].”
Background
l-Citrulline Metabolism in Mice Augments CD4+ T Cell Proliferation and Cytokine Production In Vitro, and Accumulation in the Mycobacteria-Infected Lung
Lange, S., McKell, M. C., Schmidt, S., Hossfeld, A. P., Chaturvedi, V., Kinder, J. M., McAlees, J. W., Lewkowich, I. P., Way, S. S., Turner, J., et al. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01561 · Cited by 25
“org November 2017 | Volume 8 | Article 1561 Previous data have shown that loss of Arg1 leads to improved mycobacterial host defense early, but allows T cell-mediated immunopathology in late stages of infection (21, 30), reminding us that regulating a balance of activation and inhibition is a key property during immune…”
BackgroundSelf-citation
Myeloid HIF‐1α regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection
Resende, M., Ferreira, C. M., Barbosa, A. M., Cardoso, M. S., Sousa, J., Saraiva, M., Castro, A. G., Appelberg, R., & Torrado, E. (2019) · Immunology · doi:10.1111/imm.13131 · Cited by 25
Liver-specific knockout of arginase-1 leads to a profound phenotype similar to inducible whole body arginase-1 deficiency
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Arginase 1 Insufficiency Precipitates Amyloid-β Deposition and Hastens Behavioral Impairment in a Mouse Model of Amyloidosis
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“The APP Tg2576 mice (APP), Arg1 floxed mice (Arg1), and LysMcre were bred according to the published protocol (27).”
Method
Hepatic arginase deficiency fosters dysmyelination during postnatal CNS development
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Comparative studies of macrophage-biased responses in mice to infection with Toxoplasma gondii ToxoDB #9 strains of different virulence isolated from China
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“Moreover, it is likely that at an early time of infection, with the activation of M2, the induction of Arg-1 could be exploited by TgCtwh3 to promote its growth as described previously (Figure 5) [25,26].”
Background
Arginase promotes immune evasion of Echinococcus granulosus in mice
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Trophoblast apoptosis through polarization of macrophages induced by Chinese Toxoplasma gondii isolates with different virulence in pregnant mice
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Mycobacterium tuberculosis PPE18 Protein Reduces Inflammation and Increases Survival in Animal Model of Sepsis
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“Upregulation of arginase-1 by M. tuberculosis is dependent on TLR2 and STAT-6 (80). rPPE18 is known to bind to TLR2 and induce IL-10 (21).”
Background
Trypanosomatid Infections: How Do Parasites and Their Excreted–Secreted Factors Modulate the Inducible Metabolism of l-Arginine in Macrophages?
Holzmüller, P., Geiger, A., Nzoumbou‐Boko, R., Pissarra, J., Hamrouni, S., Rodrigues, V., Dauchy, F., Lemesre, J.-L., Vincendeau, P., & Bras‐Gonçalves, R. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00778 · Cited by 23
“Toll-like receptors have been shown to impair macrophage effective immunity against intracellular pathogens through arginase 1 induction (144).”
Background
Lower Expression of Inducible Nitric Oxide Synthase and Higher Expression of Arginase in Rat Alveolar Macrophages Are Linked to Their Susceptibility to Toxoplasma gondii Infection
Zhao, Z., Zhang, J., Wei, J., Li, Z., Wang, T., Yi, S.-Q., Shen, J., Yang, T., Hide, G., & Lun, Z. (2013) · PLoS ONE · doi:10.1371/journal.pone.0063650 · Cited by 23
“gondii infection [44,45,49] and our study clearly replicates this association when comparing RPMs and RAMs.”
BackgroundResult
Turning foes into permissive hosts: manipulation of macrophage polarization by intracellular bacteria
Pham, T. H. M., & Monack, D. M. (2023) · Current Opinion in Immunology · doi:10.1016/j.coi.2023.102367 · Cited by 22
Mild Hyperthermia Accelerates Bone Repair by Dynamically Regulating iNOS/Arg1 Balance in the Early Stage
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The Role of gp130 Cytokines in Tuberculosis
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“During mycobacterial infection, Arg1 derived from AAM counteracts protective macrophage effector mechanisms [152,156,157].”
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Progress and Prospects of Regulatory Functions Mediated by Nitric Oxide on Immunity and Immunotherapy
Hu, Q., Shi, J., Zhang, J., Wang, Y., Guo, Y., & Zhang, Z. (2021) · Advanced Therapeutics · doi:10.1002/adtp.202100032 · Cited by 22
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“Others have shown in response to Mycobacterium tuberculosis and Toxoplasma gondii, that specific ablation of Arg1 in Mø improved immunity to these pathogens through increased NO production (El Kasmi et al., 2008).”
Background
MAP Kinase Phosphatase-2 Plays a Key Role in the Control of Infection with Toxoplasma gondii by Modulating iNOS and Arginase-1 Activities in Mice
Woods, S., Schroeder, J., McGachy, H. A., Plevin, R. J., Roberts, C. W., & Alexander, J. K. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003535 · Cited by 21
“Previously it has been suggested that arginase-1 stimulates parasite growth by converting L-arginine to the polyamines needed by the parasite [32] or inhibiting iNOS activity by Larginine depletion [33].”
BackgroundInfluential
Itaconate, Arginine, and Gamma-Aminobutyric Acid: A Host Metabolite Triad Protective Against Mycobacterial Infection
Kim, J. K., Park, E., & Jo, E. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.832015 · Cited by 21
“ARG1 elimination in macrophages reduces the bacterial load in the lung during Mtb infection (62).”
Background
There is no direct competition between arginase and nitric oxide synthase for the common substrate l-arginine.
Momma, T. Y., & Ottaviani, J. (2022) · Nitric oxide · doi:10.1016/j.niox.2022.09.002 · Cited by 19
Chitin induces upregulation of B7‐H1 on macrophages and inhibits T‐cell proliferation
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Macrophages as a Battleground for Toxoplasma Pathogenesis
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“However, infection of macrophage-specific Arg1 conditional knockouts with a type II strain is strongly protective in terms of survival (El Kasmi et al., 2008).”
BackgroundSelf-citation
Initial cytoplasmic and phagosomal consequences of human neutrophil exposure to Staphylococcus epidermidis
Bernardo, J., Long, H. J., & Simons, E. R. (2009) · Cytometry Part A · doi:10.1002/cyto.a.20827 · Cited by 22
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Endostatin gene therapy inhibits intratumoral macrophage M2 polarization
Foguer, K., Braga, M. D. S., Peron, J. P. S., Bortoluci, K. R., & Bellini, M. H. (2016) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2016.01.035 · Cited by 22
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Method
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Genetic background affects the expansion of macrophage subsets in the lungs of Mycobacterium tuberculosis ‐infected hosts
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C1QTNF3 is Upregulated During Subcutaneous Adipose Tissue Remodeling and Stimulates Macrophage Chemotaxis and M1-Like Polarization
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“org 10 this may appear surprising, increased Arg1 expression is seen in LPS-stimulated murine macrophages, possibly as a mean to attenuate NO-mediated inflammation (42, 43).”
Background
Mycobacterium tuberculosis suppresses host antimicrobial peptides by dehydrogenating L-alanine
Peng, C., CHENG, Y. N., Ma, M., Qiu, C., Duan, Y., Liu, S., Cheng, H., Yang, H., Huang, J., Bu, W., et al. (2024) · Nature Communications · doi:10.1038/s41467-024-48588-4 · Cited by 20
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“of intracellular arginine, which is a substrate required to produce microbicidal NO (40, 41).”
Background
Natural resistance to worms exacerbates bovine tuberculosis severity independently of worm coinfection
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Background
Pneumocystis infection alters the activation state of pulmonary macrophages
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“El Kasmi and colleagues demonstrated that in intracellular infection models in mice lacking arginase-1 expression, NO production is enhanced, resulting in reduced bacterial burdens and lower morbidity to both Mycobacterium species and Toxoplasma gondii (El Kasmi et al., 2008).”
BackgroundInfluential
Bovine viral diarrhea virus type 2 in vivo infection modulates TLR4 responsiveness in differentiated myeloid cells which is associated with decreased MyD88 expression
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Authors: El Kasmi, K. C., Qualls, J. E., Pesce, J. T., Smith, A. M., Thompson, R. W., Henao-Tamayo, M., Basaraba, R. J., König, T., Schleicher, U., Koo, M.-S., Kaplan, G., Fitzgerald, K. A., Tuomanen, E. I., Orme, I. M., Kanneganti, T.-D., Bogdan, C., Wynn, T. A., & Murray, P. J.
Affiliations: St. Jude Children's Research Hospital (US)
National Institutes of Health (US)
Colorado State University (US)
University Medical Center Freiburg (DE)
Universitätsklinikum Erlangen (DE)
University of Medicine and Dentistry of New Jersey (US)
University of Massachusetts Chan Medical School (US)
Corresponding author: Wynn, Thomas A
Murray, Peter J
ORCID: Qualls, Joseph E
Smith, Amber M
Henao-Tamayo, Marcela
Basaraba, Randall J
Schleicher, Ulrike
Fitzgerald, Katherine A
Tuomanen, Elaine I
Kanneganti, Thirumala-Devi
Bogdan, Christian
Wynn, Thomas A
Murray, Peter J
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2008-11-02
Volume: 9
Issue: 12
Pages: 1399-1406
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.1671
PMC: PMC2584974
OpenAlex: W2038461328
Cited by: 646
References: 50
Citations by year: 2026: 18 · 2025: 20 · 2024: 19 · 2023: 33 · 2022: 25 · 2021: 48 · 2020: 34 · 2019: 35 · 2018: 32 · 2017: 29 · 2016: 52 · 2015: 51 · 2014: 52 · 2013: 49 · 2012: 39
FWCI: 13.66
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship@UMassChan (submittedVersion)
Funders: National Institutes of Health
National Cancer Institute (P30CA021765)
National Institute of Allergy and Infectious Diseases (AI27913, R01AI027913, AI062921, R01AI066046, AI66046, R01AI062921)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
Keywords: arginase-1, Toll-like receptor signaling, macrophages, intracellular pathogens, Mycobacterium tuberculosis, Toxoplasma gondii, nitric oxide, STAT6, host-pathogen interaction, tuberculosis, toxoplasmosis, lung bacterial load
MeSH terms: Animals, Arginase, Bacterial Infections, Immunohistochemistry, Macrophages, Immunoblotting, Mice, Knockout, CCAAT-Enhancer-Binding Protein-beta, STAT6 Transcription Factor, Toll-Like Receptors, Mice, Myeloid Differentiation Factor 88

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Toll-like receptor–induced arginase 1 in macrophages thwarts effective immunity against intracellular pathogens

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