IL17A and pulmonary fibrosis: These results demonstrate that comorbidity was able to alter the immune response, which provides a profibrogenic environment, and allows us to elucidate and assume as a shortcoming of our study that if it were maintained longer, elevated levels of IL-17A and TGF-β1 could also have been observed, as well as increased collagen deposition, thereby contributing to pulmonary fibrosis.