ArticleInfection and immunity2011
MyD88 signaling is required for efficient innate and adaptive immune responses to Paracoccidioides brasiliensis infection.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 76 citations in OpenAlex.
- Polymorphism in the Promoter Region of theFrontiers in immunology · 2020Trial
- Advances in Elucidating the Mitochondrial DNA Mechanisms Underlying Ozone-Induced Inflammation.Toxics · 2026Review
- Combined anti-PD-1 and amphotericin B therapy reduces fungal burden and enhances control of murine paracoccidioidomycosis.Frontiers in cellular and infection microbiology · 2026Article
- Extracellular vesicles from virulentVirulence · 2024Article
- C-type lectin receptor expression is a hallmark of neutrophils infiltrating the skin in epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- Myeloid-derived suppressor cells are associated with impaired Th1 and Th17 responses and severe pulmonary paracoccidioidomycosis which is reversed by anti-Gr1 therapy.Frontiers in immunology · 2023Article
- Foreign body response to synthetic polymer biomaterials and the role of adaptive immunity.Biomedical materials (Bristol, England) · 2022Review
- The Role of IL-17-Producing Cells in Cutaneous Fungal Infections.International journal of molecular sciences · 2021Review
- Paracoccidioidomycosis Protective Immunity.Journal of fungi (Basel, Switzerland) · 2021Review
- Effect of LPS and LTA stimulation on the expression of TLR-pathway genes in PBMCs of Akkaraman lambs in vivo.Tropical animal health and production · 2021Article
- Integrative Analysis of Human Macrophage Inflammatory Response Related toFrontiers in immunology · 2021Article
- AhR Ligands Modulate the Differentiation of Innate Lymphoid Cells and T Helper Cell Subsets That Control the Severity of a Pulmonary Fungal Infection.Frontiers in immunology · 2021Article
- Pulmonary paracoccidioidomycosis in AhR deficient hosts is severe and associated with defective Treg and Th22 responses.Scientific reports · 2020Article
- Review
- The Role of the Interleukin-17 Axis and Neutrophils in the Pathogenesis of Endemic and Systemic Mycoses.Frontiers in cellular and infection microbiology · 2020Review
- Regulatory T cells in paracoccidioidomycosis.Virulence · 2019Review
- Myeloid Differentiation Factor 88 and Interleukin-1R1 Signaling Contribute to Resistance to Coccidioides immitis.Infection and immunity · 2018Article
- Innate Immunity against Cryptococcus, from Recognition to Elimination.Journal of fungi (Basel, Switzerland) · 2018Review
- TLR3 Is a Negative Regulator of Immune Responses AgainstFrontiers in cellular and infection microbiology · 2018Article
- Induction of Hypergammaglobulinemia and Autoantibodies byFrontiers in immunology · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms that govern the initial interaction between Paracoccidioides brasiliensis, a primary dimorphic fungal pathogen, and cells of the innate immunity need to be clarified. Our previous studies showed that Toll-like receptor 2 (TLR2) and TLR4 regulate the initial interaction of fungal cells with macrophages and the pattern of adaptive immunity that further develops. The aim of the present investigation was to assess the role of MyD88, an adaptor molecule used by TLRs to activate genes of the inflammatory response in pulmonary paracoccidioidomycosis. Studies were performed with normal and MyD88(-/-) C57BL/6 mice intratracheally infected with P. brasiliensis yeast cells. MyD88(-/-) macrophages displayed impaired interaction with fungal yeast cells and produced low levels of IL-12, MCP-1, and nitric oxide, thus allowing increased fungal growth. Compared with wild-type (WT) mice, MyD88(-/-) mice developed a more severe infection of the lungs and had marked dissemination of fungal cells to the liver and spleen. MyD88(-/-) mice presented low levels of Th1, Th2, and Th17 cytokines, suppressed lymphoproliferation, and impaired influx of inflammatory cells to the lungs, and this group of cells comprised lower numbers of neutrophils, activated macrophages, and T cells. Nonorganized, coalescent granulomas, which contained high numbers of fungal cells, characterized the severe lesions of MyD88(-/-) mice; the lesions replaced extensive areas of several organs. Therefore, MyD88(-/-) mice were unable to control fungal growth and showed a significantly decreased survival time. In conclusion, our findings demonstrate that MyD88 signaling is important in the activation of fungicidal mechanisms and the induction of protective innate and adaptive immune responses against P. brasiliensis.
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