Cited by 571Inflammasome and immune disordersTuberculosis Research and EpidemiologyImmune Response and Inflammation

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Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome–dependent processing of IL-1β

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Mishra, Bibhuti B, Rathinam, Vijay A K, Martens, Gregory W, Martinot, Amanda J, Kornfeld, Hardy, Fitzgerald, Katherine A, Sassetti, Christopher M·2013·Nature Immunology

DOI 10.1038/ni.2474PMC PMC3721324

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Abstract

Interleukin 1 (IL-1) is an important mediator of innate immunity but can also promote inflammatory tissue damage. During chronic infections such as tuberculosis, the beneficial antimicrobial role of IL-1 must be balanced with the need to prevent immunopathology. By exogenously controlling the replication of Mycobacterium tuberculosis in vivo, we obviated the requirement for antimicrobial immunity and discovered that both IL-1 production and infection-induced immunopathology were suppressed by lymphocyte-derived interferon-γ (IFN-γ). This effect was mediated by nitric oxide (NO), which we found specifically inhibited assembly of the NLRP3 inflammasome via thiol nitrosylation. Our data indicate that the NO produced as a result of adaptive immunity is indispensable in modulating the destructive innate inflammatory responses elicited during persistent infections.

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Authors: Mishra, B. B., Rathinam, V. A. K., Martens, G. W., Martinot, A. J., Kornfeld, H., Fitzgerald, K. A., & Sassetti, C. M.
Affiliations: University of Massachusetts Chan Medical School (US)
Harvard University (US)
Howard Hughes Medical Institute (US)
Corresponding author: Sassetti, Christopher M
ORCID: Mishra, Bibhuti B
Rathinam, Vijay A K
Martinot, Amanda J
Kornfeld, Hardy
Fitzgerald, Katherine A
Sassetti, Christopher M
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2012-11-18
Volume: 14
Issue: 1
Pages: 52-60
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2474
PMC: PMC3721324
OpenAlex: W2048884877
Cited by: 571
References: 49
Citations by year: 2026: 24 · 2025: 27 · 2024: 29 · 2023: 39 · 2022: 47 · 2021: 53 · 2020: 46 · 2019: 43 · 2018: 51 · 2017: 46 · 2016: 46 · 2015: 40 · 2014: 40 · 2013: 37 · 2012: 3
FWCI: 15.44
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: Howard Hughes Medical Institute
National Heart, Lung, and Blood Institute (R01HL064884, R01HL081149, HL064884)
National Institute of Allergy and Infectious Diseases (AI064282, R01AI064282, AI083713, U54AI057159, R01AI083713, T32AI007638)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: nitric oxide, NLRP3 inflammasome, interleukin-1β processing, tuberculosis, immunopathology, Mycobacterium tuberculosis, nitrosylation, interferon-gamma, innate immunity, chronic infection, adaptive immunity
MeSH terms: NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Cells, Cultured, Humans, Immunity, Innate, Interferon-gamma, Mice, Inbred C57BL, Mycobacterium tuberculosis, Nitric Oxide, Tuberculosis, Signal Transduction, Mice, Knockout, Protein Modification, Translational, Mice, Interleukin-1beta, Protein Multimerization, Inflammasomes

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Nitric oxide controls the immunopathology of tuberculosis by inhibiting NLRP3 inflammasome–dependent processing of IL-1β

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