Mycobacterium tuberculosis and the host cell inflammasome: a complex relationship
Open accessAbstract
The production of IL-1β during the infection with Mycobacterium tuberculosis (Mtb) is important for successful host immune defense. In macrophages and dendritic cells the host cell inflammasome is crucial for generation of secreted IL-1β in response to Mtb infections. In these cell types Mtb infection only activates the NLRP3-inflammasome. New reports demonstrate that nitric oxide has an important function in the negative regulation of the NLRP3-inflammasome to reduce tissue damage during Mtb infections. The type I interferon, IFN-β, is induced after Mtb infections and can also suppress NLRP3-inflammasome activation. In contrast, IFN-β increases activity of the AIM2-inflammasome after infection with intracellular pathogens such as Francisella tularensis and Listeria monocytogenes. Recent results demonstrate that non-tuberculous mycobacteria but not virulent Mtb induce the AIM2-inflammasome in an IFN-β dependent matter. Indeed, Mtb inhibits AIM2-inflammasome activation via its ESX-1 secretion system. This novel immune evasion mechanism may help Mtb to allow the induction of low levels of IFN-β to suppress the NLRP3-inflammasome without activating the AIM2-inflammasome.
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M. tuberculosis reduces inflammasome activation by inducing IFN-β, thereby contributing to immune evasion.
“M. tuberculosis is capable of reducing this activation pathway by inducing the formation of IFN-β, thereby contributing to immune evasion of the bacterium (100).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [100]
Formation of IL-1β and IL-18 from pro-IL-1β and pro-IL-18β is dependent on activation of the inflammasome and caspase-1.
“The formation of IL-1β as well as of IL-18 from pro- IL-1β and pro-Il18β, respectively, is dependent on the activation of the inflammasome and of caspase-1 (100).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [100]
During M. tuberculosis infection, inflammasome activation is controlled by NLRP3.
“During M. tuberculosis infection inflammasome activation is controlled by the nucleotide binding and oligomerization domain, leucine rich-containing proteins 3 (NLRP3).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [100]
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- Authors
- Briken, V., Ahlbrand, S. E., & Shah, S.
- Affiliations
- University of Maryland, College Park (US)
- Corresponding author
- Briken, Volker
- Venue
- Frontiers in Cellular and Infection Microbiology
- Publisher
- Frontiers Media SA
- Published
- 2013
- Volume
- 3
- Pages
- 62-62
- ISSN
- 2235-2988 (ISSN-L)
- PMC
- PMC3793174
- OpenAlex
- W2003754055
- Cited by
- 92
- References
- 76
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 11 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 12 · 2019: 9 · 2018: 10 · 2017: 12 · 2016: 7 · 2015: 8 · 2014: 8
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Cellular and Infection Microbiology (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
- National Institutes of Health (AI072584)
- National Institute of Allergy and Infectious Diseases (AI072584, R56AI072584, R01AI072584, T32AI089621)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- Mycobacterium tuberculosis, NLRP3 inflammasome, AIM2 inflammasome, IL-1β, nitric oxide, type I interferon, interferon-beta, ESX-1 secretion system, immune evasion, nontuberculous mycobacteria, macrophages, dendritic cells, Francisella tularensis, Listeria monocytogenes
- MeSH terms
- Dendritic Cells, Macrophages, Mycobacterium tuberculosis, Host-Pathogen Interactions, Immune Evasion, Inflammasomes
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