Adaptive stress response induced by toluene increases Sporothrix schenckii virulence and host immune response

Environmental factors modify the physiology of microorganisms, allowing their survival in extreme conditions. However, the influence of chemical contaminants on fungal virulence has been little studied. Sporotrichosis is an emergent fungal disease caused by Sporothrix schenckii, a soil-inhabiting fu...

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Published inbioRxiv
Main Authors Tellez-Martinez, Damiana, Batista-Duharte, Alexander, Vinicius Paschoalini Silva, Deivys Portuondo Fuentes, Lucas Souza Ferreira, Marisa Campos Polesi, Costa, Caroline Barcelos, Iracilda Zeppone Carlos
Format Paper
LanguageEnglish
Published Cold Spring Harbor Cold Spring Harbor Laboratory Press 04.02.2019
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Summary:Environmental factors modify the physiology of microorganisms, allowing their survival in extreme conditions. However, the influence of chemical contaminants on fungal virulence has been little studied. Sporotrichosis is an emergent fungal disease caused by Sporothrix schenckii, a soil-inhabiting fungus that has been found in polluted environments. Here, we evaluated the adaptive stress response of S. schenckii induced by toluene, a key soil contaminant. The effect on fungal virulence and host immune response was also assessed. The fungus survived up to 0.10% toluene in liquid medium. Greater production of melanosomes and enhanced activity superoxide dismutase, associated to increased tolerance to H2O2 were observed in toluene-exposed fungi. Intraperitoneal infection of mice with S. schenckii treated with either 0, 0.01 or 0.1% of toluene, resulted in greater fungal burden at day 7 post-infection in spleen and liver in the groups infected with fungus treated with toluene 0.1%. A higher production of Il-1β, TNF-α, IL-10 and nitric oxyde by peritoneal macrophages and IFNγ, IL-4 and IL-17 by splenocytes was also observed in that group. Our findings showed that morphological and functional changes induced by toluene leads to increased S. schenckii virulence and antifungal host immune response in our model.
DOI:10.1101/539775