ArticlePloS one2012
Activation of an NLRP3 inflammasome restricts Mycobacterium kansasii infection.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
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- Interaction of Mycobacteria With Host Cell Inflammasomes.Frontiers in immunology · 2022Review
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- The Roles of Inflammasomes in Host Defense againstPathogens (Basel, Switzerland) · 2021Review
- Mechanism of action and potential applications of selective inhibition of microsomal prostaglandin E synthase-1-mediated PGEScientific reports · 2021Article
- Effect and Mechanism ofBioMed research international · 2021Article
- Immune defects in patients with pulmonaryERJ open research · 2020Article
- Macrophage Signaling Pathways in Pulmonary Nontuberculous Mycobacteria Infections.American journal of respiratory cell and molecular biology · 2020Review
- Cytolethal distending toxin-induced release of interleukin-1β by human macrophages is dependent upon activation of glycogen synthase kinase 3β, spleen tyrosine kinase (Syk) and the noncanonical inflammasome.Cellular microbiology · 2020Article
- Internalization and Intoxication of Human Macrophages by the Active Subunit of theFrontiers in immunology · 2020Article
- Role of Mitochondria in the Redox Signaling Network and Its Outcomes in High Impact Inflammatory Syndromes.Frontiers in endocrinology · 2020Review
- NLRP3 inflammasome is attenuated in patients with Mycobacterium avium complex lung disease and correlated with decreased interleukin-1β response and host susceptibility.Scientific reports · 2019Article
- Brucella abortus nitric oxide metabolite regulates inflammasome activation and IL-1β secretion in murine macrophages.European journal of immunology · 2019Article
- The Association of Childhood Maltreatment With Lipid Peroxidation and DNA Damage in Postpartum Women.Frontiers in psychiatry · 2019Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium kansasii has emerged as an important nontuberculous mycobacterium pathogen, whose incidence and prevalence have been increasing in the last decade. M. kansasii can cause pulmonary tuberculosis clinically and radiographically indistinguishable from that caused by Mycobacterium tuberculosis infection. Unlike the widely-studied M. tuberculosis, little is known about the innate immune response against M. kansasii infection. Although inflammasome activation plays an important role in host defense against bacterial infection, its role against atypical mycobacteria remains poorly understood. In this report, the role of inflammasome activity in THP-1 macrophages against M. kansasii infection was studied. Results indicated that viable, but not heat-killed, M. kansasii induced caspase-1-dependent IL-1β secretion in macrophages. The underlying mechanism was found to be through activation of an inflammasome containing the NLR (Nod-like receptor) family member NLRP3 and the adaptor protein ASC (apoptosis-associated speck-like protein containing a CARD). Further, potassium efflux, lysosomal acidification, ROS production and cathepsin B release played a role in M. kansasii-induced inflammasome activation. Finally, the secreted IL-1β derived from caspase-1 activation was shown to restrict intracellular M. kansasii. These findings demonstrate a biological role for the NLRP3 inflammasome in host defense against M. kansasii.
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