MYD88 and inflammatory response: However, in mice with acute lung injury (ALI), overexpression of miR-27a by agomir-27a improved lung injury and ameliorated lung inflammation via decreasing TLR4/MyD88/NF-κB activation, evidenced by decreased levels of TNF-α, IL-6, IL-1β, and myeloperoxidase (MPO) activity in bronchoalveolar lavage fluid [29].