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Biomedical subjects

B J Rathbone

Publications and source records attributed to B J Rathbone.

48 records · Page 3Linked to original sources
PubMed1988

Possible pathogenetic pathways of Campylobacter pylori in gastro-duodenal disease.

The exact pathogenic mechanisms involved in Campylobacter pylori associated gastro-duodenal inflammation are unclear. C. pylori adheres to gastric type epithelium and colonisation is associated with a number of ultrastructural abnormalities. Other factors thought important include the marked bacterial urease activity, enzymatic degradation of the mucous layer and possible toxins. The induced inflammatory reaction will also contribute to tissue damage and a breakdown of normal defense mechanisms.

Antibody Formation↗
PubMed1988

Immune response of the gastric mucosa to Campylobacter pylori.

The histological features of non-autoimmune chronic gastritis are consistent with those of a local immune response by the gastric mucosa. If Campylobacter pylori is causative in this condition, then the immune response will be in part specific for this organism. Antibodies to C. pylori are present in the gastric juice of infected patients. Coating of mucosal C. pylori by antibody in vivo can be demonstrated by immunohistochemistry, and a neutrophil infiltrate (active gastritis) is associated with coating by opsonising antibodies. Gastric mucosa from patients with C. pylori produces specific immunoglobulin in vitro, and this antibody production correlates with the plasma cell infiltrate seen in these patients. Lymphoid follicles in gastric mucosa, implying local antigenic stimulation, are a specific feature of campylobacter-associated gastritis. The inflammation gradually abates following eradication of the bacteria. We conclude that the morphological features of campylobacter-associated gastritis represent the immune response of the mucosa to C. pylori.

Antibodies, Bacterial↗
PubMed1987

Campylobacter pyloridis and acid induced gastric metaplasia in the pathogenesis of duodenitis.

Biopsy specimens of gastric and duodenal mucosa from 290 patients were examined histologically for metaplasia and Campylobacter pyloridis. Estimates of pH on samples of fasting gastric juice from 55 of the patients were performed, and mucosal biopsy specimens from 33 patients were also cultured for C pyloridis. Active duodenitis was seen in 34 duodenal biopsy specimens. Thirty (88%) of the patients with active duodenitis had both greater than 5% gastric metaplasia in the duodenal specimen and C pyloridis associated gastritis. These two factors coexisted in only 0.43% of patients with no duodenal inflammation. When C pyloridis were seen histologically in duodenal biopsy specimens they were confined to areas of gastric metaplasia and never occurred in the absence of a polymorph infiltrate. Of the 55 patients with measurements of gastric juice pH, gastric metaplasia was present in the duodenum in 20 of 42 with a pH of less than 2.5, and in 0 of 13 with a pH of greater than 2.5. These results suggest that acid induced gastric metaplasia in the duodenum and C pyloridis associated gastritis may be synergistic in the pathogenesis of duodenitis; the metaplastic gastric epithelium allows C pyloridis to colonise the duodenal mucosa, where it produces an acute inflammatory response.

Adolescent↗
PubMed1986

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

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.

Antibodies, Bacterial↗
PubMed1986

Local immune response to gastric Campylobacter in non-ulcer dyspepsia.

Colonising Campylobacter pyloridis were identified histologically in gastric biopsy specimens from 89% of 83 patients with non-ulcer dyspepsia and chronic gastritis, but not in 58 dyspeptic patients with normal mucosa. The presence and population density of organisms was associated with the presence of intraepithelial neutrophils. In vivo coating of the organisms by host immunoglobulin was investigated by immunoperoxidase staining of IgA, IgG, and IgM in 54 biopsy specimens. IgA coated bacteria were seen in all cases of active gastritis, and in 60% of biopsy specimens without intraepithelial neutrophils. Coating with IgG or IgM, or both, was correlated with activity of gastritis and was rarely seen in the absence of a neutrophil infiltrate.

Adult↗