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Cited by 220

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 access
Nouailles, Geraldine, Dorhoi, Anca, Koch, Markus, Zerrahn, Jens, Weiner, January, Faé, Kellen C., Arrey, Frida, Kuhlmann, Stefanie, Bandermann, Silke, Loewe, Delia, Mollenkopf, Hans-Joachim, Vogelzang, Alexis, Meyer-Schwesinger, Catherine, Mittrücker, Hans-Willi, McEwen, Gayle, Kaufmann, Stefan H.E.·2014·Journal of Clinical Investigation

Abstract

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.

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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

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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

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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.