Revisiting the pathogenesis of dermatophytosis: A cross‐sectional analytic study of serum levels of interleukins‐2, 8, 10 and 17

Abstract

AbstractBackgroundGiven the current epidemic‐like scenario of dermatophyte infections, it is prudent to revisit the immunopathogenesis of dermatophytosis. Comprehending the intricate interactions among interleukins can aid in understanding the recent trends in infection. There is a paucity of literature on the various cytokine levels observed in the serum of patients suffering from various dermatophytoses.AimTo study serum cytokine levels of interleukins 2, 8, 10 and 17 in patients with dermatophytosis.MethodsA cross‐sectional analytic study was conducted on 64 cases of clinical dermatophyte infections (KOH confirmed) and 64 controls. The clinico‐epidemiological profile of the cases was studied. By using a solid phase sandwich ELISA (enzyme‐linked immunosorbent assay), the serum levels of interleukins 2, 8, 10 and 17 were measured and compared between cases and controls. Serum interleukin‐2, 8, 10 and 17 levels were studied among cases based on mode of onset, duration of illness, treatment history, site of infection and multiple other morphological characteristics of the infection.ResultsThe cases had statistically higher levels of interleukins‐8, 10 and 17 in comparison with controls. The levels of interleukin‐8 were significantly lower (p < .05) among those who had received oral antifungals. In cases where the lesion had scaling, the serum levels of interleukin‐10 were significantly higher (p < .05). The lesional hyperpigmentation was significantly (p < .05) associated with low levels of interleukin‐17. Also, interleukin‐17 was significantly (p < .05) elevated in patients with lesions in the abdomen.ConclusionIt is the first time that serum interleukin levels are studied in dermatophytosis. There is an immunological dysfunction specific to dermatophytoses initiated by their infection. Key factor in this dysfunction is the elevation of IL‐10, contributing to persistent infection. In turn, causing an increase in IL‐17, promoting inflammation and tissue damage. This cycle of elevated IL‐10 and IL‐17 can further exacerbate the infection and lead to chronicity. The activity of IL‐2 and the Th1 immune pathway is reduced by two opposing immune pathways: the Th17 and Th2 axes.