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The aetiology of the irritable bowel syndrome (IBS) is incompletely understood. A low-grade colonic inflammation is frequently seen, but it is unclear to what extent this phenomenon contributes to the pathophysiology of IBS. CD4+CD25+ regulatory T cells (Treg) are implicated to play an important role in suppressing intestinal inflammation. We, therefore, examined whether the intestinal inflammatory process in IBS patients is the result of an altered function and/or frequency of CD25+ Treg cells. Patients with IBS ( n = 34), fulfilling the Rome II criteria, were compared with controls ( n = 26). The suppressive activity of blood CD25+ Treg cells was determined and the frequency of colonic and blood CD25+ Treg cells was analysed by flow cytometry. The expression of the Treg marker, FOXP3 mRNA, in colonic biopsies was determined by reverse transcription-polymerase chain reaction. Blood CD25+ Treg cells from IBS patients suppressed the proliferation of blood CD4+CD25low/− T cells. Similar frequencies of CD25+ Treg cells were recorded in mucosa and blood of IBS patients and controls. FOXP3 mRNA was equally expressed in the colonic mucosa of patients with IBS and controls. In conclusion, the low-grade intestinal inflammation recorded in patients with IBS is not associated with an altered function or frequency of CD25+ Treg cells. [ABSTRACT FROM AUTHOR]

Background: Neuromodulation may be a new therapeutic approach in inflammatory bowel disease, but very little is known about neural control of colonic secretion in vivo. We therefore determined the effects of neural blockade on colonic motor activity and mucosal secretion in anaesthetized rats. Methods: A proximal and a distal colonic segment were isolated in four groups of chloralose-anaesthetized rats (n = 8 in each group), and we measured luminal pressure and transmural potential difference (PD) as a marker of electrogenic chloride secretion. Recordings were made from proximal and distal segments simultaneously, which made it possible to directly compare response patterns. Results: Under control conditions luminal pressure waves were associated with phasic, lumen-negative increases in PD which had a significantly greater magnitude and longer duration in the distal colon. Atropine blocked both pressure waves and PD waves in the proximal colon, but some PD waves, although of lower magnitude, remained in the distal colon. Hexamethonium abolished pressure waves in both segments and induced a marked reduction in PD in the distal but not in the proximal colon. Lidocaine also reduced PD, more so in the distal colon, and dissociated the pressure-PD linkage. Conclusion: In the distal but not in the proximal colon, there is a strong nicotinic, neurogenic `tone' that maintains a high basal secretory activity. The results encourage the search for neuromodulatory agents in the treatment of colonic secretory disease. [ABSTRACT FROM AUTHOR]

In 17 healthy volunteers, we studied the dynamics of secretory immunoglobulin A (SIgA) release in the proximal small intestine (distal duodenum and proximal jejunum), using a modified triple-lumen perfusion technique. Secretory data were related to the current phase of the migrating motor complex (MMC), as recorded by manometry. In both segments, luminal SIgA output changed cyclically, with peak outputs occurring at the end of the MMC cycle (late phase II). These MMC-related changes were due to two factors: cyclic inflow of SIgA from more proximal sites, and a cyclic release of SIgA from the test segment that correlated in time with an increase in epithelial fluid secretion. Cyclic intestinal SIgA release may thus be another secretory component of the MMC. The data are compatible with the hypothesis that motility and SIgA release are linked by motility-activated chloride secretion from the intestinal crypts. [ABSTRACT FROM AUTHOR]