Helicobacter pylori is a gastric pathogen that colonizes approximately 50% of the world's population. Infection with H. pylori causes chronic inflammation and significantly increases the risk of developing duodenal and gastric ulcer disease and gastric cancer. Infection with H. pylori is the strongest known risk factor for gastric cancer, which is the second leading cause of cancer-related deaths worldwide. Once H. pylori colonizes the gastric environment, it persists for the lifetime of the host, suggesting that the host immune response is ineffective in clearing this bacterium. In this review, we discuss the host immune response and examine other host factors that increase the pathogenic potential of this bacterium, including host polymorphisms, alterations to the apical-junctional complex, and the effects of environmental factors. In addition to host effects and responses, H. pylori strains are genetically diverse. We discuss the main virulence determinants in H. pylori strains and the correlation between these and the diverse clinical outcomes following H. pylori infection. Since H. pylori inhibits the gastric epithelium of half of the world, it is crucial that we continue to gain understanding of host and microbial factors that increase the risk of developing more severe clinical outcomes.

Helicobacter pylori and Gastric Cancer: Factors That Modulate Disease Risk

Campylobacter pylori detected noninvasively by the 13C-urea breath test.

Campylobacter pyloridis is a spiral bacterium which was seen by histopathologists several years before it was cultured in 1982 in Perth, Western Australia. It has unique cellular fatty acids, predominantly tetradecanoic acid and cis-11, 12 methylene octadecanoic acid. It also has a unique ultrastructure which is different from that of other campylobacters. C pyloridis possesses a powerful urease enzyme and produces large amounts of extracellular catalase. Both these features may be important virulence factors, allowing it to occupy a protected niche in the stomach below the mucus layer but above the gastric mucosa. Specific lesions are found in the gastric mucosa, and ultrastructural studies show the presence of adherence pedestals identical with those found with enteropathogenic Escherichia coli of the intestine. Histological examination of gastric biopsy tissue has shown that C pyloridis is strongly associated with active chronic gastritis, when polymorphonuclear leucocytes are present, and is not found on normal mucosa except when a biopsy specimen from elsewhere in the stomach shows active chronic gastritis. When patients with symptoms caused by gastritis are identified dual antibacterial treatment, combining the action of bismuth in the stomach with a systemic antibiotic, can eradicate C pyloridis, with remission of symptoms and restoration of normal epithelial morphology. Most peptic ulcers relapse after modern acid reducing treatment, and antibacterial treatment may be beneficial in preventing relapse.

https://jcp.bmj.com/content/jclinpath/39/4/353.full.pdf

Campylobacter pyloridis, gastritis, and peptic ulceration.

https://www.gastrojournal.org/article/0016-5085(92)90126-J/pdf

Hypotheses on the pathogenesis and natural history of Helicobacter pylori-induced inflammation

Campylobacter pylori infection has been recognized as being strongly associated with chronic gastritis and duodenal ulceration, but the prevalence of C. pylori infection in a normal population is not known. A serological survey was conducted in four countries with different geographical and socioeconomic status, in a randomly chosen population as representative as possible, by using an enzyme-linked immunosorbent assay (ELISA) with a sonic extract of two strains as the antigen. The test had a specificity of 94% when 600 ELISA units was used as the threshold. In France, few children were infected before the age of 10 years. The prevalence then increased gradually to 36.7% in the sixth decade of life. This increasing prevalence of infection with age was also observed in Algeria, Vietnam, and the Ivory Coast but at a higher rate (80 to 90%). In Vietnam, as in France, few children were infected, whereas in Africa, C. pylori infection occurred earlier. The prevalence of infection did not differ with sex for a particular age group; it also did not differ with respect to gastric symptoms, smoking and drinking habits, or urban or rural residence when these potential risk factors were studied. The epidemiological data available on peptic ulcer disease in developing countries compared with developed countries led to the speculation that infection with C. pylori is not a sufficient condition to develop this disease.

Seroepidemiology of Campylobacter pylori infection in various populations.

Antibody titres to Campylobacter pyloridis in serum and gastric juice were estimated by an enzyme linked immunosorbent assay (ELISA) to whole organisms obtained from bacterial culture in 39 patients with non-ulcer dyspepsia Whereas 20 of the 21 patients with chronic gastritis had gastric C pyloridis, 17 patients with no C pyloridis had normal histology in the gastric antrum and body Significantly raised serum IgG and IgA antibody titres to C pyloridis were found in colonised patients with gastritis Patients with raised IgG antibody to C pyloridis were also shown to have significantly raised titres to other Campylobacter species, suggesting antigenic cross reactivity Gastric juice antibodies were also studied and IgA titres to C pyloridis were detected in a proportion of patients with gastritis, together with low levels of IgM, but no IgG

https://gut.bmj.com/content/gutjnl/27/6/642.full.pdf

B W Worsley

Papers

Systemic and local antibody responses to gastric Campylobacter pyloridis in non-ulcer dyspepsia.

Immune response to campylobacter pyloridis

Alimentary tract andpancreas Systemic andlocal antibody responses togastric Campylobacterpyloridis innon-ulcer dyspepsia