Moreover, a recent study suggested that the modulation of monocyte recruitment and endothelial activation during LPS-induced endotoxemia are mediated by MCP-1 [50], and another study by Katherine et al. showed that antibody neutralization of MCP-1 in a mouse model of sepsis leads to greatly decreased transcription of IL-1α, IL-1β, and IL-6 in the diaphragm [51]. The gene discussed is CCL2; the disease is serum lipopolysaccharide activity.