Pathogenic mechanisms of postinfectious functional gastrointestinal disorders: Results 3 years after gastroenteritis

Objective. Functional gastrointestinal disorders (FGID) may appear after acute gastroenteritis. The aim of this study was to evaluate the possible mechanisms ( inflammation, visceral hypersensitivity, psychological and immunogenetic factors) related to the development of postinfectious ( PI) FGID 3 years after a Salmonella outbreak. Material and methods. Biopsies of the antrum, and right- and left colon from 16 PI-FGID patients, 8 PI control patients, and 18 healthy controls (H-controls) were processed for immunohistochemistry, cytokines, and mast-cell electron microscopy. DNA was typed for cytokine gene polymorphisms. Visceral sensitivity ( satiety test and rectal barostat) and psychological factors (SCL-90 and vital events) were assessed. Results. The number of mast cells and T lymphocytes was similar among the groups in all locations. Mast cells within 5 mu m of nerve fibers of both PI groups were increased compared to H-controls: ( stomach: 5.6 +/- 1.2 versus 6.6 +/- 1.5 versus 2.5 +/- 1.1; right colon: 9.7 +/- 1.3 versus 8.0 +/- 1.3 versus 4.1 +/- 1.7; left colon: 8.9 +/- 0.9 versus 8.5 +/- 1.8 versus 2.2 +/- 2.0 per field) (p<0.05). No differences in the production of IL-1 beta, IL-1ra, IL-6, and IL-10 or in their genotypes were found. PI-FGID patients showed a lower pain threshold to rectal distention (29 +/- 2 versus 37 +/- 2 mmHg; p<0.05). Scores for anxiety (0.63 +/- 0.11 versus 0.28 +/- 0.14) and somatization (1.01 +/- 0.15 versus 0.45 +/- 0.15) were higher in PI-FGID patients than in PI controls (p<0.05). The number of stressful life events was not significantly different between both PI groups. Conclusions. Three years after salmonellosis, PI-FGID patients showed no evidence of inflammation in the gastric or colonic mucosa, but visceral sensitivity and anxiety/somatization levels were increased. The close anatomical mast cell-nerve fibers relation does not seem to be related to the FGID but to the infection itself.