RESPIRABLE SIRNA TARGETING AT THE NF-KB PATHWAY PROTECTS AGAINST INFLAMMATORY LUNG DISEASES

Abstract

Asthma and chronic obstructive pulmonary disease (COPD) are common inflammatory pulmonary diseases. Cumulative evidences have shown the role of NF-kB signaling pathway in the pathogenesis of asthma and COPD. Ribosomal protein S3 (RPS3) is a subunit of NF-kB complex while receptor-interacting protein 2 (Rip2) is a positive upstream regulator of NF-kB pathway. In my PhD projects, I sought to investigate if RPS3 and Rip2 siRNA could protect against HDM-induced mouse asthma model or CS-induced mouse COPD model. RPS3 and Rip2 siRNA markedly knocked down RPS3 and Rip2 levels in mouse cell lines and mouse lung. RPS3 siRNA abated HDM-induced mucus hypersecretion, cytokine production, and serum IgE elevation. RPS3 and Rip2 siRNA ameliorated neutrophil infiltration and suppressed CS-induced inflammatory and oxidative damage marker levels. Here we reported that RPS3 and Rip2 siRNA ameliorated lung inflammation via the interruption of NF-kB activity, postulating the therapeutic potential of them.