Relationship of single nucleotide polymorphisms (SNPs) of the CARD9 gene with fungal infections caused by Trichophyton rubrum in diabetic patients.

Abstract

Trichophyton rubrum is the main causative agent of superficial mycoses in Brazil and worldwide. Currently, there is a considerable increase in dermatophytosis in immunocompromised patients, in which these lesions can be more penetrating and invasive, making treatment difficult. The innate immune system acts as the first line of defense against dermatophyte infection and is regulated by pattern recognition receptors (PRRs). These include Toll-like receptors (TLRs) and Dectin-1 receptors (Member of the C-type lectin receptor family - CLRs), which detect mannans present in the fungal cell wall. The CARD9 gene is involved in signaling and activating the innate immune response to fungi via PRRs, regulating inflammation through the release of cytokines. Host genetic factors, such as mutations in the genes encoding PRRs and the CARD9 gene, may be related to fungal infections caused by T. rubrum. Furthermore, studies show that diabetic patients are more susceptible to infections such as those caused by fungi due to immune dysfunction. These cases of deep and recurrent fungal infections have increased the search for new genetic studies to elucidate the dermatophyte-host relationship. The objective of this project is to evaluate the genetic susceptibility to fungal infections of patients with dermatophytosis caused by T. rubrum through genotyping of the CARD gene. In addition to isolating clinical samples of T. rubrum and characterizing the sensitivity profile to antifungals, in order to understand the mechanisms of dermatophyte-host interaction.