RE: Marsden Anti-microbial conference31 Aug 2022 09:37
They should try putting in directly in to the lungs.
[28,29], this pathway could represent a mechanism, how fungal priming of IFN-I responses builds antiviral countermeasures. Given the potential of commensal Candida species to induce IFN-I responses [8,10,20], it may be worth investigating, whether their colonization shape smucosal antiviral immunity.5. Is IFN-I immunotherapy an option?Immunotherapy is an increasingly recognized essential strategy to improve the outcome of fungal infections. These therapies either can augment a compromised immune system or sup-press detrimental inflammatory responses. Thus, this is particularly attractive for infections inimmuno compromised patients or infections associated with immunopathology.The capacity of IFN-I to improve several aspects of antifungal host defense warrants their exploration as candidates for immunotherapy of mucosal fungal infections.Particularly, treatment of VVC is complex due to the interplay between fungal pathogenic-ity and immunopathology underlying its pathogenesis. While immunotherapy for VVC hasnot yet been broadly explored, IFNawas successful in increasing resistance to VVC in a rat model [22]. Besides, IFN-I treatment can have diverse beneficial effects during VVC by increasing epithelial resistance to infection [20,22] and inhibiting detrimental inflammatory responses [20]. This evidence suggesting a protective role of IFN-I at mucosal barriers supports that specifically mucosal, rather than systemic, disease may benefit from such therapy. Con-cerning aspergillosis, chronic granulomatous disease (CGD) patients are another group that potentially could ultimately benefit from IFN-I immunotherapy, as IFN-I-inducing poly I:Ctreatment in mice neutrophil-dependent improved outcome of aspergillosis [30]. Further-more, exogenous IFN-I administration rescued inadequate antifungal responses in dectin-1-/-mice [16]. IFN-I signaling is well documented for its role in maintaining intestinal barrier homeostasis. Therefore, it is tempting to speculate that IFN-I immunotherapy may be a valu-able approach to reduce C.albicans translocation through improving epithelial barrier func-tion. It is, however, difficult to estimate how such an immunotherapy affects immunocompromised patients. Yet in the context of inflammatory bowel diseases (IBDs),IFN-I are discussed as an immunomodulatory treatment strategy. Given the evidence for a key role of C.albicans pathogenicity mechanisms in IBD [31], IFN-I therapy may both modulate inflammatory responses and increase epithelial resistance to fungal pathogenicity. IFN-I medi-ate cross-talk between epithelial cells and the immune system during commensalism and infection, potentially making them an attractive therapeutic target for fungal infections in the gut, lung, and vaginal mucosa.
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