The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis
Open accessAbstract
Successful host defense against numerous pulmonary infections depends on bacterial clearance by polymorphonuclear leukocytes (PMNs); however, excessive PMN accumulation can result in life-threatening lung injury. Local expression of CXC chemokines is critical for PMN recruitment. The impact of chemokine-dependent PMN recruitment during pulmonary Mycobacterium tuberculosis infection is not fully understood. Here, we analyzed expression of genes encoding CXC chemokines in M. tuberculosis-infected murine lung tissue and found that M. tuberculosis infection promotes upregulation of Cxcr2 and its ligand Cxcl5. To determine the contribution of CXCL5 in pulmonary PMN recruitment, we generated Cxcl5(-/-) mice and analyzed their immune response against M. tuberculosis. Both Cxcr2(-/-) mice and Cxcl5(-/-) mice, which are deficient for only one of numerous CXCR2 ligands, exhibited enhanced survival compared with that of WT mice following high-dose M. tuberculosis infection. The resistance of Cxcl5(-/-) mice to M. tuberculosis infection was not due to heightened M. tuberculosis clearance but was the result of impaired PMN recruitment, which reduced pulmonary inflammation. Lung epithelial cells were the main source of CXCL5 upon M. tuberculosis infection, and secretion of CXCL5 was reduced by blocking TLR2 signaling. Together, our data indicate that TLR2-induced epithelial-derived CXCL5 is critical for PMN-driven destructive inflammation in pulmonary tuberculosis.
Overview
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
Verification
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.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Smyth, G. K. (2004) · Statistical Applications in Genetics and Molecular Biology · doi:10.2202/1544-6115.1027 · Cited by 11,829
GOrilla: a tool for discovery and visualization of enriched GO terms in ranked gene lists
Eden, E., Navon, R., Steinfeld, I., Lipson, D., & Yakhini, Z. (2009) · BMC Bioinformatics · doi:10.1186/1471-2105-10-48 · Cited by 3,356
A novel signaling pathway impact analysis
Tarca, A. L., Draghici, S., Khatri, P., Hassan, S. S., Mittal, P., Kim, J.-S., Kim, C. J., Kusanovic, J. P., & Romero, R. (2009) · Bioinformatics · doi:10.1093/bioinformatics/btn577 · Cited by 1,031
Bafica, A., Scanga, C. A., Feng, C. G., Leifer, C., Cheever, A., & Sher, A. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20051782 · Cited by 601
Neutrophil-mediated innate immune resistance to mycobacteria
Martineau, A. R., Newton, S. M., Wilkinson, K. A., Kampmann, B., Hall, B. M., Nawroly, N., Packe, G. E., Davidson, R. N., Griffiths, C. J., & Wilkinson, R. J. (2007) · Journal of Clinical Investigation · doi:10.1172/jci31097 · Cited by 394
Chou, R. C., Kim, N. D., Sadik, C. D., Seung, E., Lan, Y., Byrne, M. H., Haribabu, B., Iwakura, Y., & Luster, A. D. (2010) · Immunity · doi:10.1016/j.immuni.2010.07.018 · Cited by 342
Neutrophils in tuberculosis: friend or foe?
Lowe, D. M., Redford, P. S., Wilkinson, R. J., O’Garra, A., & Martineau, A. R. (2012) · Trends in Immunology · doi:10.1016/j.it.2011.10.003 · Cited by 312
Yang, C.-T., Cambier, C. J., Davis, J. M., Hall, C. J., Crosier, P. S., & Ramakrishnan, L. (2012) · Cell Host & Microbe · doi:10.1016/j.chom.2012.07.009 · Cited by 293
Corleis, B., Korbel, D., Wilson, R., Bylund, J., Chee, R., & Schaible, U. E. (2012) · Cellular Microbiology · doi:10.1111/j.1462-5822.2012.01783.x · Cited by 150
Lionakis, M. S., Fischer, B. G., Lim, J. K., Swamydas, M., Wan, W., Richard Lee, C.-C., Cohen, J. I., Scheinberg, P., Gao, J.-L., & Murphy, P. M. (2012) · PLoS Pathogens · doi:10.1371/journal.ppat.1002865 · Cited by 118 · cited 1×
“Both CXCR2 and CCR1 function as neutrophil chemokine receptors (28, 29, 48, 49).”
Cited by
An expansion of rare lineage intestinal microbes characterizes rheumatoid arthritis
Chen, J., Wright, K., Davis, J. M., Jeraldo, P., Marietta, E. V., Murray, J., Nelson, H., Matteson, E. L., & Taneja, V. (2016) · Genome Medicine · doi:10.1186/s13073-016-0299-7 · Cited by 858
Innate immunity in tuberculosis: host defense vs pathogen evasion
Liu, C. H., Liu, H., & Ge, B. (2017) · Cellular & Molecular Immunology · doi:10.1038/cmi.2017.88 · Cited by 532
Immunology of Mycobacterium tuberculosis Infections
Sia, J. K., & Rengarajan, J. (2019) · Microbiology Spectrum · doi:10.1128/microbiolspec.gpp3-0022-2018 · Cited by 312
Nitric oxide prevents a pathogen-permissive granulocytic inflammation during tuberculosis
Mishra, B. B., Lovewell, R. R., Olive, A. J., Zhang, G., Wang, W., Eugenin, E., Smith, C. M., Phuah, J. Y., Long, J. E., Dubuke, M. L., et al. (2017) · Nature Microbiology · doi:10.1038/nmicrobiol.2017.72 · Cited by 284
Sirt3 promotes antimycobacterial defenses by coordinating mitochondrial and autophagic functions
Kim, T. S., Jin, Y. B., Kim, Y. S., Kim, S., Kim, J. K., Lee, H.-M., Suh, H.-W., Choe, J. H., Kim, Y. J., Koo, B.-S., et al. (2019) · Autophagy · doi:10.1080/15548627.2019.1582743 · Cited by 172
Metadata
- Authors
- Nouailles, G., Dorhoi, A., Koch, M., Zerrahn, J., Weiner, J., Faé, K. C., Arrey, F., Kuhlmann, S., Bandermann, S., Loewe, D., Mollenkopf, H.-J., Vogelzang, A., Meyer-Schwesinger, C., Mittrücker, H.-W., McEwen, G., & Kaufmann, S. H. E.
- Venue
- Journal of Clinical Investigation
- Published
- 2014-02-10
- Volume
- 124
- Issue
- 3
- Pages
- 1268-1282
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2094735775
- Cited by
- 220
- References
- 10
- FWCI
- 14.49
- Type
- journal article
- Language
- en
- Open access
- bronze
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis. https://app.cochat.ai/papers/10.1172/jci72030
- The paper
- Nouailles, G., Dorhoi, A., Koch, M., Zerrahn, J., Weiner, J., Faé, K. C., Arrey, F., Kuhlmann, S., Bandermann, S., Loewe, D., Mollenkopf, H.-J., Vogelzang, A., Meyer-Schwesinger, C., Mittrücker, H.-W., McEwen, G., & Kaufmann, S. H. E. (2014). CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis. Journal of Clinical Investigation. https://doi.org/10.1172/jci72030
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.