Lipocalin 2 Regulates Inflammation during Pulmonary Mycobacterial Infections
Open accessAbstract
Pulmonary tuberculosis (TB), caused by the intracellular bacteria Mycobacterium tuberculosis, is a worldwide disease that continues to kill more than 1.5 million people every year worldwide. The accumulation of lymphocytes mediates the formation of the tubercle granuloma in the lung and is crucial for host protection against M.tuberculosis infection. However, paradoxically the tubercle granuloma is also the basis for the immunopathology associated with the disease and very little is known about the regulatory mechanisms that constrain the inflammation associated with the granulomas. Lipocalin 2 (Lcn2) is a member of the lipocalin family of proteins and binds to bacterial siderophores thereby sequestering iron required for bacterial growth. Thus far, it is not known whether Lcn2 plays a role in the inflammatory response to mycobacterial pulmonary infections. In the present study, using models of acute and chronic mycobacterial pulmonary infections, we reveal a novel role for Lcn2 in constraining T cell lymphocytic accumulation and inflammation by inhibiting inflammatory chemokines, such as CXCL9. In contrast, Lcn2 promotes neutrophil recruitment during mycobacterial pulmonary infection, by inducing G-CSF and KC in alveolar macrophages. Importantly, despite a common role for Lcn2 in regulating chemokines during mycobacterial pulmonary infections, Lcn2 deficient mice are more susceptible to acute M.bovis BCG, but not low dose M.tuberculosis pulmonary infection.
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Increased susceptibility of Lcn2−/− mice to mycobacterial infections might be due to Lcn2's function as a chemoattractant for neutrophils rather than iron sequestration.
“Importantly, Lcn2−/− mice are more susceptible to mycobacterial infections (214), which might be different from the iron-sequestrating role of Lcn2 (215) but rather due to its function as efficient chemoattractant for neutrophils to sites of infection (216–218).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [216]
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- [19]Johnson EE, Srikanth CV, Sandgren A, Harrington L, Trebicka E, et al (2010) Siderocalin inhibits the intracellular replication of Mycobacterium tuberculosis in macrophages. FEMS Immunol Med Microbiol 58: 138– 145. 19863663 PMC2822896
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- Authors
- Guglani, L., Gopal, R., Rangel-Moreno, J., Junecko, B. F., Lin, Y., Berger, T., Mak, T. W., Alcorn, J. F., Randall, T. D., Reinhart, T. A., Chan, Y. R., & Khader, S. A.
- Affiliations
- University of Pittsburgh (US)
- University Health Network (CA)
- University of Rochester Medicine (US)
- Corresponding author
- Khader, Shabaana A.
- ORCID
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2012-11-20
- Volume
- 7
- Issue
- 11
- Pages
- e50052
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3502292
- OpenAlex
- W2168982702
- Cited by
- 68
- References
- 37
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 8 · 2022: 8 · 2021: 8 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 5 · 2016: 3 · 2015: 10 · 2014: 3 · 2013: 4
- FWCI
- 3.75
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- University of Pittsburgh
- U.S. Public Health Service (A1083541)
- Medical Center, University of Pittsburgh
- National Heart, Lung, and Blood Institute (HL105427-01, R01HL105427)
- National Institute of Allergy and Infectious Diseases (R21AI083541)
- Children's Hospital of Pittsburgh
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- neutrophil gelatinase-associated lipocalin, pulmonary tuberculosis, Mycobacterium tuberculosis, Mycobacterium bovis BCG, inflammation regulation, T cell accumulation, CXCL9, chemokines, neutrophil recruitment, granulocyte colony-stimulating factor, KC chemokine, alveolar macrophages, iron metabolism, host defense
- MeSH terms
- Lipocalin-2, Acute Disease, Acute-Phase Proteins, Animals, Cell Movement, Chronic Disease, Inflammation, Iron, Mice, Inbred C57BL, Mycobacterium bovis, Mycobacterium Infections, Mycobacterium tuberculosis, Neutrophils, T-Lymphocytes, Tuberculosis, Oncogene Proteins, Granuloma, Respiratory Tract, Gene Expression, Macrophages, Alveolar, Siderophores, Mice, Knockout, Mice, Chemokine CXCL9, Lipocalins
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