Heterogeneous expression of human cathelicidin hCAP18/LL-37 in inflammatory bowel diseases.
Schauber. Jürgen J; Rieger. Daniel D; Weiler. Frank F; Wehkamp. Jan J; Eck. Matthias M; Fellermann. Klaus K; Scheppach. Wolfgang W; Gallo. Richard L RL; Stange. Eduard F EF
Key Findings
- LL‑37 levels are significantly increased in both inflamed and non‑inflamed colon tissue of ulcerative colitis patients
- s disease tissue regardless of inflammation or NOD2 status",
Practical Outcomes
- For DIY health enthusiasts, the data imply that boosting LL‑37 may not be necessary for ulcerative colitis since it’s already elevated, while Crohn's patients might have a relative deficiency. However, the study provides no clear method to raise LL‑37, so any supplementation strategy would be speculative at this stage.
Summary
The study found that the antimicrobial peptide LL‑37 is higher in the colon tissue of ulcerative colitis patients, but stays the same in Crohn's disease patients. Lab tests showed that common inflammation signals and the short‑chain fatty acid butyrate didn’t change LL‑37 levels in colon cells. This suggests the body’s natural LL‑37 response differs between the two gut diseases.
Abstract
Inflammatory bowel diseases (IBDs) are characterized by a breakdown of colon epithelial barrier function. Antimicrobial peptides like cathelicidins are molecules of the innate immune system located at epithelial surfaces. Cathelicidins influence microbial growth and inflammation and may play a role in IBD. In this study, the expression of human cathelicidin hCAP18/LL-37 was investigated in the intestinal mucosa from patients suffering from ulcerative colitis or Crohn's disease. Biopsy material from colon and ileal mucosa of a total of 89 patients (34 with Crohn's disease, 27 with ulcerative colitis, 28 control patients) was evaluated for cathelicidin expression by real-time reverse-transcriptase polymerase chain reaction and immunohistochemistry. Colon epithelial cells were stimulated in vitro with various cytokines to evaluate mechanisms that influence cathelicidin production. Cathelicidin expression was significantly increased in inflamed and non-inflamed colon mucosa from ulcerative colitis patients compared to non-inflamed control mucosa. In patients with Crohn's disease cathelicidin expression was not changed in inflamed or non-inflamed colon or ileal mucosa independent of NOD2 status. Biopsies evaluated by immunohistochemistry showed epithelial cathelicidin expression in the upper crypt that was diffuse in controls and only basal in IBD patients. Inflammation mediators, alone or in combination with the known cathelicidin inducer butyrate, had no effect on cathelicidin expression in cultured colon cells. In IBD the colonic expression of human cathelicidin is altered: cathelicidin expression is increased in inflamed and non-inflamed mucosa in patients suffering from ulcerative colitis but not in Crohn's disease. This deficiency may further compromise the antimicrobial barrier in Crohn's disease.
Study Information
pubmed
2006
2006-06-01T00:00:00.000Z
10.1097/00042737-200606000-00007
154
37