Gastric acid secretion appears to be an important mechanism which reduces the viable bacterial load of any contaminated food, although it is partially redundant in the typical Western diet, which is relatively sterile. This is relevant in food-allergic individuals, in whom gastric mucosal absorption of antigen can stimulate vomiting, which acts to remove the offending antigen. Antigen challenge stimulates gastric acid secretion in sensitised animals and delays gastric emptying 2,3 . These mechanisms denature potential antigen, delaying contact with the small intestinal mucosa, but also have relevance for an understanding of the role of the stomach in limiting microbial access to the small intestine. The stomach's defences do, however, fail to prevent colonisation with Helicobacter pylori , which is now recognised to survive effectively in gastric mucosa and induce chronic active gastritis 4 .
Attachment occurs to epithelial cells and to mucus.
Recent evidence suggests that in childhood infection the failure to eliminate H. pylori , with resulting atrophic gastritis and impaired gastric acid secretion, may lead to bacterial overgrowth of the small bowel or colonisation with enteric pathogens 5 . H. pylori has also been shown to be a risk factor for subsequent development of adenocarcinoma of the stomach 6 . The small intestinal mucosa is modified to maximise its surface area through mucosal folds, villi and microvilli. Barrier function has been best studied in this region. Simplistically, the small intestinal epithelium may be regarded as consisting of a continuous sheet of enterocytes joined around their circumferences by a specialised structure termed the junctional complex.