Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology

doi:10.1016/0140-6736(91)90477-7

The Lancet

Volume 338, Issue 8763, 10 August 1991, Pages 332-335

https://doi.org/10.1016/0140-6736(91)90477-7 Get rights and content

Abstract

The gastric IgA response to Helicobacter pylori was examined in 100 dyspeptic patients by means of immunoblotting of supernatants from antral biopsy and gastric mononuclear cell cultures. 76 of 78 patients with chronic gastritis, 2 of 8 with reactive gastritis, and 1 of 14 subjects with normal mucosa showed positive responses. Of patients with chronic gastritis, 75%, 83%, 97%, and 76%, respectively, showed responses to the 120 kDa, 90 kDa, 61 kDa, and 31 kDa proteins. None of the 19 patients with chronic gastritis who did not recognise the 120 kDa protein had peptic ulcers, whereas 25 of 57 with positive recognition had peptic ulcers (p<0·001). Mucosal recognition of the Hpylori 120 kDa protein was also positively associated with the activity of gastritis (polymorph infiltration) (p<0·002) and with the extent of surface degeneration (p<0·01). These findings suggest that 120-kDa-positive strains of H pylori have pathogenic features associated with active gastritis and peptic ulceration. Infection with 120-kDa-negative strains may explain why peptic ulceration develops in only a proportion of subjects infected with H pylori.

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Mucosal IgA recognition of Helicobacter pylori 120 kDa protein, peptic ulceration, and gastric pathology

Abstract

Gastroenterology

Zbl Bakt Hyg A

Lancet

Lancet

Lancet

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Lancet

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J Clin Pathol

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Scand J Gastroenterol

Campylobacter pylori and non-ulcer dyspepsia

Pathogenesis of infection by Hpylori

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Infect Immun

Immunoblot analysis of immune response to Campylobacter pylori and its clinical associates

J Clin Pathol