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The discovery of antimicrobial peptides has extended our knowledge of non‐specific defence mechanisms. In addition to the physical barrier, the intestinal epithelium contributes to host defence by producing antimicrobial peptides to limit access to enteric bacteria and other microorganisms.1 The production of inducible antimicrobial peptides offers an initial rapid defence response of epithelial cells against invading microbes.2
Human β‐defensin‐2 (HBD‐2) was the first inducible human antimicrobial protein discovered.3 It can be induced by probiotic microorganisms and pro‐inflammatory cytokines.4 Recent results suggest that HBD‐2 is expressed in active intestinal inflammation, especially in ulcerative colitis.5 Thus far, the expression of β‐defensins has been quantified in the intestinal mucosa using the polymerase chain reaction procedure. Our aim was to evaluate faecal measurements of HBD‐2 in patients with active ulcerative colitis, compared with irritable bowel syndrome as a non‐inflammatory clinical control and with healthy controls. We expected that faecal HBD‐2 levels would show a similar pattern to mucosal HBD‐2 and thus be selectively increased in ulcerative colitis.
Faecal specimens were collected from 69 patients (22 with active ulcerative colitis, 24 with irritable bowel syndrome, and 23 healthy controls) (table 11).). To avoid any influence of probiotics in our data, patients on probiotic drugs were excluded. Further exclusion criteria for the patients with irritable bowel syndrome were a raised C‐reactive protein or leucocyte count and a history of infectious gastrointestinal disease or bacterial overgrowth over the previous six months. Disease status was addressed in all participating subjects by medical history and current symptoms. In addition, each patient with irritable bowel syndrome or ulcerative colitis underwent ileocolonoscopy with histopathology. Faecal HBD‐2 was measured by enzyme linked immunosorbent assay (Immundiagnostik, Bensheim, Germany) and reported as ng/g faeces. HBD‐2 concentrations (mean (SD)) were 104.9 (62.9) ng/g in the active ulcerative colitis group, 72.9 (52.9) ng/g in the irritable bowel syndrome group, and 31.0 (15.4) ng/g in the healthy controls (p<0.0005). Scheffé post hoc tests showed significant differences between healthy controls and the two patient groups (fig 11).
The results first imply that levels of HBD‐2 are detectable in faeces and can be quantified. Second, as in mucosal specimens, HBD‐2 levels are significantly raised in faeces in patients with ulcerative colitis compared with healthy controls. Finally, in contrast to our hypothesis, faecal levels of HBD‐2 were significantly raised in patients with irritable bowel syndrome compared with healthy controls and were similar to those in the patients with ulcerative colitis. These results suggest activation of the mucosal innate defence system towards a proinflammatory response in patients with irritable bowel syndrome, in the absence of macroscopic signs of inflammation.
Inflammatory conditions of the gastrointestinal tract—including inflammatory bowel disease and acute gastrointestinal infections—are associated with disturbed intestinal motor function and decreased sensory thresholds.6 These sensorimotor abnormalities are not necessarily related to an overt inflammatory reaction as they can occur even when inflammation is minimal and is restricted to the mucosa.6 Thus altered sensory and motor function accompanied by the development of symptoms suggestive of irritable bowel syndrome has been observed in patients with quiescent ulcerative colitis.7 First support for a possible involvement of intestinal inflammation in irritable bowel syndrome was based on observations of increased numbers of mast cells in the muscularis externa8 or a significant increase in lamina propria immune cells in the colonic mucosa of affected patients,9 and has been under discussion since. Nonetheless, the general consensus is that irritable bowel syndrome is a non‐inflammatory disease.
In conclusion, this is the first study to present preliminary data on faecal HBD‐2 levels in patients with irritable bowel syndrome, ulcerative colitis, and healthy controls. In contrast to our hypotheses, our findings support a proinflammatory response of the mucosal innate defence system in irritable bowel syndrome. The functional significance of these findings remains to be elucidated.
Conflict of interest: None declared.