Abstract
IL-19 is a member of IL-10 family and is mainly produced by macrophages. Acute pancreatitis (AP) is an inflammatory disease characterized by acinar cell injury and necrosis. In the present study, the role of IL-19 in AP and AP-associated lung injury in mice was explored using L-arginine-induced pancreatitis. Experimental pancreatitis was induced by intraperitoneal injection of L-arginine in wild-type (WT) and IL-19 gene-deficient (IL-19 KO) mice. Among the mice treated with L-arginine, the serum amylase level was significantly increased in the IL-19 KO mice, and interstitial edema, analyzed using hematoxylin and eosin-stained sections, was aggravated mildly in IL-19 KO mice compared with WT mice. Furthermore, the mRNA expression of tumor necrosis factor-α was significantly upregulated in IL-19 KO mice treated with L-arginine compared with WT mice treated with L-arginine. IL-19 mRNA was equally expressed in the pancreases of both control and L-arginine-treated WT mice. The conditions of lung alveoli were then evaluated in WT and IL-19 KO mice treated with L-arginine. In mice with L-arginine-induced pancreatitis, the alveolar area was remarkedly decreased, and expression of lung myeloperoxidase was significantly increased in IL-19 KO mice compared with WT mice. In the lungs, the mRNA expression of IL-6 and inducible nitric oxide synthase was significantly increased in IL-19 KO mice compared with WT mice. In summary, IL-19 was proposed to alleviate L-arginine-induced pancreatitis by regulating TNF-α production and to protect against AP-related lung injury by inhibiting neutrophil migration.