Mahesh Manjunath Gouda and Yashodhar Prabhakar Bhandary
Acute lung injury is the severe health issue characterized by inflammation in the airways results in the alteration of alveolar architecture. The inflammatory phase usually mediated by the neutrophil accumulation, migration of macrophages, alveolar infiltration and cytokines activation. IL-17A is a class of pro-inflammatory cytokines elevated during the initial phase of injury. IL-17A mediation could alter various pathways such as, alveolar epithelial cells (AECs) apoptosis, chemokines enhancement and excitation as well as other proliferatory pathways. IL-17A mediated activation of chemokines expression is one of the key phenomenon promotes the inflammatory process. IL-17A mediated downstream modulation leads to the severe form of injury, which causes the significant loss of AECs. The severe loss of AECs stimulates the conversion of fibroblasts to myofibroblasts and deposition of extracellular matrix (ECM). The excess deposition of ECM at the alveolar epithelial barrier causes the thickening of alveolar epithelium and results in the progression of lethal, irreversible disease called pulmonary fibrosis.
