ArticleInfection and immunity2014
Pathogenic fungus Microsporum canis activates the NLRP3 inflammasome.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- Loss-of-function CARD8 mutation causes NLRP3 inflammasome activation and Crohn's disease.The Journal of clinical investigation · 2018Trial
- Extracellular Vesicles fromJournal of fungi (Basel, Switzerland) · 2026Article
- Prevalence of dermatophyte infections in cats in Ramadi and Fallujah Cities, Iraq.Open veterinary journal · 2025Article
- IL-18 production is required for the generation of a Th1 response during experimental chromoblastomycosis.PloS one · 2025Article
- Antifungal activity ofFrontiers in microbiology · 2024Article
- The role of NLRP1 and NLRP3 inflammasomes in the etiopathogeneses of pityriasis lichenoides chronica and mycosis fungoides: an immunohistochemical study.Archives of dermatological research · 2023Article
- Antifungal activity ofCurrent medical mycology · 2023Article
- Dermatophyte infection: from fungal pathogenicity to host immune responses.Frontiers in immunology · 2023Review
- CARD9 Regulation and its Role in Cardiovascular Diseases.International journal of biological sciences · 2022Review
- [Kerion Celsi due to Microsporum canis infection].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2021Review
- Aim2 Couples With Ube2i for Sumoylation-Mediated Repression of Interferon Signatures in Systemic Lupus Erythematosus.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
- Role of inflammasomes/pyroptosis and PANoptosis during fungal infection.PLoS pathogens · 2021Review
- Interplays between inflammasomes and viruses, bacteria (pathogenic and probiotic), yeasts and parasites.Immunology letters · 2020Review
- The adaptor protein CARD9, from fungal immunity to tumorigenesis.American journal of cancer research · 2020Review
- Article
- Skin Immunity to Dermatophytes: From Experimental Infection Models to Human Disease.Frontiers in immunology · 2020Review
- FSH1 regulates the phenotype and pathogenicity of the pathogenic dermatophyte Microsporum canis.International journal of molecular medicine · 2019Article
- NLRP3 inflammasome activation from Kupffer cells is involved in liver fibrosis of Schistosoma japonicum-infected mice via NF-κB.Parasites & vectors · 2019Article
- Fosfomycin Protects Mice FromFrontiers in cellular and infection microbiology · 2019Article
- MicroRNA Post-transcriptional Regulation of the NLRP3 Inflammasome in Immunopathologies.Frontiers in pharmacology · 2019Review
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Microsporum canis is a pathogenic fungus with worldwide distribution that causes tinea capitis in animals and humans. M. canis also causes invasive infection in immunocompromised patients. To defy pathogenic fungal infection, the host innate immune system is the first line of defense. As an important arm of innate immunity, the inflammasomes are intracellular multiprotein complexes that control the activation of caspase-1, which cleaves proinflammatory cytokine pro-interleukin-1β (IL-1β) into its mature form. To determine whether the inflammasome is involved in the host defense against M. canis infection, we challenged human monocytic THP-1 cells and mouse dendritic cells with a clinical strain of M. canis isolated from patients with tinea capitis. We found that M. canis infection triggered rapid secretion of IL-1β from both THP-1 cells and mouse dendritic cells. Moreover, by using gene-specific shRNA and competitive inhibitors, we determined that M. canis-induced IL-1β secretion was dependent on NLRP3. The pathways proposed for NLRP3 inflammasome activation, namely, cathepsin B activity, K(+) efflux, and reactive oxygen species production, were all required for the inflammasome activation triggered by M. canis. Meanwhile, Syk, Dectin-1, and Card9 were found to be involved in M. canis-induced IL-1β secretion via regulation of pro-IL-1β transcription. More importantly, our data revealed that M. canis-induced production of IL-1β was dependent on the NLRP3 inflammasome in vivo. Together, this study unveils that the NLRP3 inflammasome exerts a critical role in host innate immune responses against M. canis infection, and our data suggest that diseases that result from M. canis infection might be controlled by regulating the activation of inflammasomes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.