Epithelium related deposition of activated complement in Helicobacter pylori associated gastritis

• Published in: Gut 1997-02, Vol.40 (2), p.196-203
• Main Authors: Berstad, A E, Brandtzaeg, P, Stave, R, Halstensen, T S
• Format: Article
• Language: English
• Subjects: Adult; Aged; Aged, 80 and over; Bacterial diseases; Bacterial diseases of the digestive system and abdomen; Biological and medical sciences; Chronic Disease; Complement Activation; Complement C3b - analysis; Complement Membrane Attack Complex - analysis; Epithelium - immunology; Female; Gastritis - immunology; Gastritis - microbiology; Helicobacter Infections - diagnosis; Helicobacter Infections - immunology; Helicobacter pylori; Human bacterial diseases; Humans; Immunohistochemistry; Infectious diseases; Male; Medical sciences; Microscopy, Fluorescence; Middle Aged
• ISSN: 0017-5749; 1468-3288; 1458-3288
• DOI: 10.1136/gut.40.2.196

BACKGROUND AND AIMS: It is unknown whether Helicobacter pylori infection activates complement in vivo. Mucosal deposition of various activation products of the complement system may contribute to the pathogenesis of chronic gastritis and was therefore studied by immunohistochemistry. PATIENTS AND METHODS: Ethanol fixed antrum or body gastric tissue sections from 24 patients infected with H pylori (determined by bacterial immunohistochemistry) and 22 uninfected patients were examined by immunofluorescence with monoclonal antibodies to activation neoepitopes in C3b and in the terminal complex (TCC). As a control group, biopsy samples from the gastric stump of 23 Billroth II operated patients were studied. RESULTS: Patchy, bright staining for TCC occurred below the surface epithelium and around the glands in H pylori positive and negative gastritis as well as in stump gastritis but seldom in normal mucosa. Activated C3 was present at the apical face of the surface epithelium, significantly more often in the antrum and body from patients with than without H pylori infection (p = 0.05 and p = 0.03 respectively), and particularly in samples with granulocyte infiltration (p = 0.04). Many bacteria were coated with activated C3 towards the pit openings but seldom within the foveolae. CONCLUSIONS: Local complement activation was shown to take place in simple chronic gastritis, associated as well as unassociated with H pylori infection, and also in stump gastritis. The fact that activated C3 was seldom seen on H pylori within the foveolae, suggested that the bacterium evades complement attack in this location.