Previous studies showed that LPS, as a key risk factor for ALI, stimulated alveolar macrophages to activate Toll-like receptor 4 (TLR4) signaling (52), while LPS could also upregulate the expression of chemokines CXCL1, CXCL2 and CCL2 on the margins of macrophages and neutrophils in the lung (53). The gene discussed is TLR4; the disease is acute respiratory distress syndrome.