As shown in Figure 6, LPS exfoliated by Bacteroidetes after death and lysis binds to LBP (LPS-binding protein, a marker of endotoxemia) and CD14 molecules on the cell surface, and further activated NF-κB signaling pathway through the TLR4 receptor on the cell membrane, promoting the expression of various pro-inflammatory factors such as TNF and IL-1β leading to systemic inflammation (Anas et al., 2010). The gene discussed is IL1B; the disease is serum lipopolysaccharide activity.