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

被引:24
|
作者
Deng, Yuan-Yuan [1 ]
Shamoon, Muhammad [1 ]
He, Yue [1 ]
Bhatia, Madhav [2 ]
Sun, Jia [1 ]
机构
[1] Jiangnan Univ, Synerget Innovat Ctr Food Safety & Nutr, Sch Food Sci & Technol, State Key Lab Food Sci & Technol, 1800 Lihu Ave, Wuxi 214122, Jiangsu, Peoples R China
[2] Univ Otago, Dept Pathol, Christchurch 8140, New Zealand
基金
中国国家自然科学基金;
关键词
immunomodulation; CRAMP; pancreatic inflammation; inflammatory mediators; INJURY; ACTIVATION; DEFENSINS; TRYPSINOGEN; APOPTOSIS; NECROSIS; THERAPY; DISEASE; CELLS; LL-37;
D O I
10.3892/mmr.2016.5008
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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-alpha 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.
引用
收藏
页码:3881 / 3885
页数:5
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