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.