{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,3]],"date-time":"2026-09-03T03:35:10Z","timestamp":1788406510264,"version":"build-2803163510"},"reference-count":65,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T00:00:00Z","timestamp":1682553600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2023,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>In the 1970s, 1% of the UK population consulted with dyspepsia; fiberoptic gastroscopy allowed biopsy specimens under direct vision enabling systematic histopathology. Steer et al described clusters of flagellated bacteria closely apposed to the gastric epithelium associated with chronic active gastritis. The first UK series of <jats:italic>Helicobacter pylori<\/jats:italic> following Marshall's 1983 visit to Worcester confirmed the association of <jats:italic>H.\u2009pylori<\/jats:italic> with gastritis. UK researchers completed much early helicobacter research as there were many UK campylobacteriologists. Steer and Newell proved the <jats:italic>Campylobacter<\/jats:italic>\u2010like organisms grown on culture were the same as those seen in the gastric mucosa using antiserum raised by inoculating rabbits with <jats:italic>H.\u2009pylori<\/jats:italic> from cultures. Wyatt, Rathbone, and others showed a strong correlation between the number of organisms, type and severity of acute gastritis, immunological response, and bacterial adhesion similar to enteropathogenic <jats:italic>E coli<\/jats:italic>. Seroprevalence studies indicated <jats:italic>H.\u2009pylori<\/jats:italic> increased with age. Histopathologists also showed peptic duodenitis was in effect \u201cgastritis in the duodenum\u201d caused by <jats:italic>H.\u2009pylori,<\/jats:italic> unifying its role in the pathogenesis of both gastritis and duodenal ulceration. These bacteria were initially called <jats:italic>Campylobacter pyloridis<\/jats:italic> and then <jats:italic>C.\u2009pylori.<\/jats:italic> However, electron microscopy suggested that the bacteria were not campylobacters, and this was supported by differences in fatty acid and polyacrylamide electrophoresis profiles. In\u2010vitro tests indicated that <jats:italic>H.\u2009pylori<\/jats:italic> was susceptible to penicillins, erythromycin, and quinolones, but not trimethoprim or cefsulodin allowing development of selective media for culture. Monotherapy with erythromycin ethylsuccinate was ineffective, and patients treated with bismuth subsalicylate initially responded with clearance of <jats:italic>H.\u2009pylori<\/jats:italic> and the associated gastritis, but then many relapsed. Thus, pharmacokinetic and treatment studies were important to direct suitable dual and triple treatments. Work optimized serology, and the rapid biopsy urease and urea breath tests. The link between <jats:italic>H.pylori<\/jats:italic> and gastric cancer was established in large seroprevalence studies, and <jats:italic>H.\u2009pylori<\/jats:italic> test and treat for dyspepsia became routine.<\/jats:p>","DOI":"10.1111\/hel.12982","type":"journal-article","created":{"date-parts":[[2023,4,27]],"date-time":"2023-04-27T11:45:02Z","timestamp":1682595902000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The first 5 years of <i>Helicobacter pylori<\/i> research\u2014With an emphasis on the United Kingdom"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4969-5360","authenticated-orcid":false,"given":"Cliodna A. 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