Abstract
Mir-10a acts in signalling pathways regulating transcription, translation, and RNA-mediated gene silencing, while IFNG acts in the T-cell receptor signalling pathway. Thus, both can be considered potential targets for understanding regulatory processes in chronic inflammation in patients with schistosomiasis. Populations in endemic areas receive mass and indiscriminate praziquantel treatment, and yet patients often have a history of multiple infections. To investigate the regulatory and prognostic capacity of miR-10 and IFNG in patient immunity, we evaluated the expression of miR-10a and IFNG as biomarkers of inflammation and their correlation with praziquantel treatment. miR-10a did not present evidence as a biomarker of inflammation in the therapeutic follow-up in schistosomiasis. However, the levels of IFNG expression were significantly higher before treatment.