ArticlePLoS neglected tropical diseases2017
Modulation of the immune response by Fonsecaea pedrosoi morphotypes in the course of experimental chromoblastomycosis and their role on inflammatory response chronicity.
Article in PLoS neglected tropical diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 31 citations in OpenAlex.
- Impaired NLRP3 inflammasome activation by chitin underlies refractory chromoblastomycosis caused byFrontiers in immunology · 2026Article
- The role of melanin inFuture microbiology · 2025Article
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- Expanding the Toolbox for Functional Genomics inJournal of fungi (Basel, Switzerland) · 2023Article
- An Experimental Model of Chromoblastomycosis Caused by Fonsecaea sp. Species.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Pathogenicity and Growth Conditions ModulateFrontiers in cellular and infection microbiology · 2022Article
- Galectin-3 Is a Crucial Immunological Disease Marker in Patients with Fungal Keratitis.Disease markers · 2022Article
- Chromoblastomycosis Due to a Never-before-Seen Dematiaceous Fungus in a Kidney Transplant Patient.Microorganisms · 2021Article
- Reviewing the Etiologic Agents, Microbe-Host Relationship, Immune Response, Diagnosis, and Treatment in Chromoblastomycosis.Journal of immunology research · 2021Review
- Muriform Cells Can Reproduce by Dividing in an Athymic Murine Model of Chromoblastomycosis due toThe American journal of tropical medicine and hygiene · 2020Article
- Early immune response against Fonsecaea pedrosoi requires Dectin-2-mediated Th17 activity, whereas Th1 response, aided by Treg cells, is crucial for fungal clearance in later stage of experimental chromoblastomycosis.PLoS neglected tropical diseases · 2020Article
- Article
- Pattern recognition receptors in fungal immunity.Seminars in cell & developmental biology · 2019Review
- An Invertebrate Host to Study Fungal Infections, Mycotoxins and Antifungal Drugs:Journal of fungi (Basel, Switzerland) · 2018Review
- Transformation of Fonsecaea pedrosoi into sclerotic cells links to the refractoriness of experimental chromoblastomycosis in BALB/c mice via a mechanism involving a chitin-induced impairment of IFN-γ production.PLoS neglected tropical diseases · 2018Article
- Flexible Signaling of Myeloid C-Type Lectin Receptors in Immunity and Inflammation.Frontiers in immunology · 2018Review
- A Model for Trans-Kingdom Pathogenicity inFrontiers in microbiology · 2018Article
- The Interaction of Human Pathogenic Fungi With C-Type Lectin Receptors.Frontiers in immunology · 2018Review
- Article
- Comparative Genomics of Sibling Species ofFrontiers in microbiology · 2017Article
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common theme across multiple fungal pathogens is their ability to impair the establishment of a protective immune response. Although early inflammation is beneficial in containing the infection, an uncontrolled inflammatory response is detrimental and may eventually oppose disease eradication. Chromoblastomycosis (CBM), a cutaneous and subcutaneous mycosis, caused by dematiaceous fungi, is capable of inducing a chronic inflammatory response. Muriform cells, the parasitic form of Fonsecaea pedrosoi, are highly prevalent in infected tissues, especially in long-standing lesions. In this study we show that hyphae and muriform cells are able to establish a murine CBM with skin lesions and histopathological aspects similar to that found in humans, with muriform cells being the most persistent fungal form, whereas mice infected with conidia do not reach the chronic phase of the disease. Moreover, in injured tissue the presence of hyphae and especially muriform cells, but not conidia, is correlated with intense production of pro-inflammatory cytokines in vivo. High-throughput RNA sequencing analysis (RNA-Seq) performed at early time points showed a strong up-regulation of genes related to fungal recognition, cell migration, inflammation, apoptosis and phagocytosis in macrophages exposed in vitro to muriform cells, but not conidia. We also demonstrate that only muriform cells required FcγR and Dectin-1 recognition to be internalized in vitro, and this is the main fungal form responsible for the intense inflammatory pattern observed in CBM, clarifying the chronic inflammatory reaction observed in most patients. Furthermore, our findings reveal two different fungal-host interaction strategies according to fungal morphotype, highlighting fungal dimorphism as an important key in understanding the bipolar nature of inflammatory response in fungal infections.
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