Basic–alimentary tractMuc1 Mucin Limits Both Helicobacter pylori Colonization of the Murine Gastric Mucosa and Associated Gastritis
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Bacterial Culture
H pylori strains SS1,5 B128, and J99 (kindly provided by Thomas Boren, Umeå University, Sweden) were initially grown on horse blood agar plates (Blood Agar Base No. 2, 0.02% Amphostat, and Skirrow’s Selective Supplements [Oxoid, Basingstoke, United Kingdom] and 5% horse blood [Biolab, Clayton, Australia]) in an anaerobic jar with a microaerophilic gas generating kit (Oxoid) for 2 days at 37°C. For infection of mice and primary cell culture adhesion assays, H pylori were cultured in brain heart
Expression of Muc1 Limits Both Acute and Chronic Colonization by H pylori
To examine the effect of Muc1 expression on colonization by gastric Helicobacters, Muc1+/+ and Muc1−/− mice were infected with H pylori-SS1 for 1 day or 1, 2, or 8 weeks before sampling of gastric tissues. Significantly, H pylori colonization in Muc1−/− mice was consistently higher compared with Muc1+/+ wild-type controls at each time point (Figure 1). The elevation in bacterial burden in the Muc1-deficient animals was remarkably constant, being between 3- to 5-fold higher from 1 day through to
Discussion
The majority of human pathogens either colonize or invade the body via a mucosal surface. The mucosal interface thus provides the first-line defensive barrier against many infections. Mucins are thought to be key components of this defense, although there is minimal experimental in vivo evidence for this dogma. Some mucins, because of their gel-forming properties, are the primary constituents of the mucus that coats mucosal surfaces, whereas others are attached to the apical surface of the
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The authors have no conflicts of interest to disclose.
Supported by Australian NHMRC Project Grants 235608 and 382309, Queensland Cancer Fund Senior Research Fellowship (to M.M.), and Australian NHMRC Project Grant 350375 (to P.S.).
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M.M. and A.E. contributed equally to this work.