The loss of ADAM17 greatly reduced the release of TNF-α and IL-6 and pulmonary leukocyte recruitment in an endotoxin-induced acute lung injury model [43], and it also inhibited the expression of p-EGFR in colonic inflammation [44] and the phosphorylation of EGFR and proinflammatory factor IL-8 expression in lipopolysaccharide-treated A549 lung epithelial cells [45]. Here, CXCL8 is linked to inflammation.