A volunteer with histologically normal gastric mucosa received pyloric campylobacter by mouth. A mild illness developed, which lasted 14 days. Histologically proven gastritis was present on the tenth day after the ingestion of bacteria, but this had largely resolved by the fourteenth day. The syndrome of acute pyloric campylobacter gastritis is described. It is proposed that this disorder may progress to a chronic infection which predisposes to peptic ulceration.
Mucous change in the human duodenum: a light and electron microscopic study and correlation with disease and gastric acid secretion
Chronic duodenitis with gastric metaplasia: electron microscopic study including comparison with normal
Different effect of Helicobacter pylori on the human gastric antral and body mucosal intracellular mucin
Prevalence of Helicobacter pylori in specific forms of gastritis. Further evidence supporting a pathogenic role for H. pylori in chronic nonspecific gastritis
Relationship between gastric inflammatory response and symptoms in patients infected with Helicobacter pylori
Prevalence of Campylobacter pylori and association with antral mucosal histology in subjects with and without upper gastrointestinal symptoms
The efficacy of antimicrobial treatment in Campylobacter pylori-associated gastritis and duodenal ulcer
Low pH activates the vacuolating toxin of Helicobacter pylori, which becomes acid and pepsin resistant.
The inflammatory response in CD1 mice shortly after infection with a CagA+/VacA+ Helicobacter pylori strain
Review article: the development of atrophic gastritis--Helicobacter pylori and the effects of acid suppressive therapy
Helicobacter pylori cagA+ strains and dissociation of gastric epithelial cell proliferation from apoptosis
Role of Helicobacter pylori infection in the incidence and clinical course of monoclonal gammopathy of undetermined significance
Relationship between Helicobacter pylori infection and gastric metaplasia in the duodenal bulb in the pathogenesis of duodenal ulcer
Clinical importance of Campylobacter pyloridis and associated serum IgG and IgA antibody responses in patients undergoing upper gastrointestinal endoscopy
Pharmacological study on the pathological changes of the gastric mucosa in Helicobacter pylori-infected Mongolian gerbils
Helicobacter pylori infection causes gastric cancer? A review of the epidemiological, meta-analytic, and experimental evidence
Helicobacter pylori vacuolating cytotoxin enters cells, localizes to the mitochondria, and induces mitochondrial membrane permeability changes correlated to toxin channel activity
Refinement of, and new applications for, Helicobacter pylori colonization in pig gastric biopsy specimens cultured in vitro
Change is good: variations in common biological mechanisms in the epsilonproteobacterial genera Campylobacter and Helicobacter
Risk Factors for Metachronous Recurrence after Endoscopic Submucosal Dissection of Early Gastric Cancer
Helicobacter pylori-induced H,K-ATPase alpha-subunit gene repression is mediated by NF-kappaB p50 homodimer promoter binding
Atrophic Gastritis is a process where gastric glandular cells are lost and replaced with firbous tissues, as a result of chronic inflammation. Learn more about Atrophic Gastritis here.
Campylobacteriosis is caused by the bacteria Campylobacter jejuni and is a common cause of gastroenteritis in humans. Discover the latest research on Campylobacteriosis here.