• gastric adenocarcinoma
• gastric inflammation
• gastric metaplasia
• enteric bacterial microflora

The gastric mucosa is exposed to billions of diverse microorganisms every day. To stymie gastric colonisation as well as to limit passage of potential pathogens to more distal segments of the GI tract, the stomach has several broadly active defence mechanisms: acidity, mucus and proteolytic enzymes. Other extragastric mechanisms may contribute: for example, glycosylation epitopes like 3′-Sulfo-Lewis A on salivary mucins cotransit with swallowed bacteria and associate with them when the pH drops in the stomach,1 presumably preventing the bacteria from binding the mucosa.

Despite these defenses, at least one bacterial species, Helicobacter pylori is able to colonise the human stomach. This pathogen initially invades the gastric antrum, but it can also spread to the gastric body by inducing a metaplastic glandular response,2 characterised by loss of acid-secreting parietal cells (oxyntic atrophy) and metaplastic glandular changes (ie, Spasmolytic Expressing Polypeptide Metaplasia or SPEM). In a small proportion of individuals, metaplasia can progress to dysplasia and gastric adenocarcinoma. Thus, identifying the early histological changes associated with H. pylori infection becomes clinically important.3

The decrease in or absence of acidity associated with oxyntic atrophy creates an environment permissive for colonisation by opportunistic microbes. Although the presence of these ectopic microbial communities correlates with oxyntic atrophy,4 previously there has been no clear demonstration that …