Cathelicidin-related antimicrobial peptide modulates the severity of acute pancreatitis in mice.

The present study aimed to investigate the immunomodulatory effects of mouse cathelicidin-related-antimicrobial peptide (CRAMP) on experimental acute-pancreatitis (AP). AP is a common clinical condition characterized-by acute abdominal inflammation. Innate immune-cells and mediators are intrinsically linked to the pathogenesis-of AP. Cathelicidins are innate immunity-derived-antimicrobial peptides that exert immunomodulatory effects-on various host cells. However, how cathelicidins are involved-and modulate the severity and inflammatory responses of AP-remains unclear. In the present study, the mouse CRAMP-gene-deficient cnlp-/- mice and their wild-type C57BL/6J-littermates were induced with AP by multiple hourly injections-of supramaximal doses of caerulein. Serum amylase-levels, pancreatic myeloperoxidase activity and histological-examination were performed in order to determine the disease-severity and the levels of inflammatory cytokines. Disease-severity and inflammatory markers were subsequently evaluated-in the control mice, cnlp-/- C57BL/6J mice with AP, and-wild-type C57BL/6J mice with AP. The results demonstrated-that cnlp-/- mice exhibited a more severe phenotype and-inflammatory response following AP induction compared-with the wild-type mice, as evidenced by increased serum-amylase levels, pancreatic myeloperoxidase release, and early-inflammatory mediator tumor necrosis factor-α production. Histological examination confirmed that CRAMP deficiency worsened the pancreatic inflammatory condition. These results indicate that CRAMP may be considered a novel modulatory mediator in mouse experimental AP. [ABSTRACT FROM AUTHOR]