Inhibitory effects of lactoferrin on pulmonary inflammatory processes induced by lipopolysaccharide by modulating the TLR4-related pathway

This study tested the ability of lactoferrin to modulate pulmonary inflammation. To construct in vitro and vivo inflammatory lung models, cells from human adenocarcinoma cell line (A549) were exposed lipopolysaccharide (LPS, 1 µg/mL), mice (CD-1) intratracheally administered LPS [10 mg/kg body weight (BW), tracheal lumen injection], respectively. The A549 preincubated with (10 mg/mL), intraperitoneally injected (100 BW), followed by treatment. concentrations proinflammatory cytokines (IL-1β TNF-α) culture medium bronchoalveolar lavage fluid determined using enzyme-linked immunosorbent assays. toll-like receptor 4–related pathway (TLR4/MyD88/IRAK1/TRAF6/NFκB) was at gene protein expression levels mouse tissue. Results showed that treatment significantly elevated IL-1β TNF-α mice; it also both mRNA expressions TLR4 downstream factors Nevertheless, apparently depressed releases tissues stimulated LPS, suppressed signaling pathway. Lactoferrin promoted enhancement miR-146a Moreover, 100°C heating for 3 min caused total loss previously listed bioactivity lactoferrin. Collectively, we proved intervened LPS-induced inflammation model model, through inhibiting TLR4-related