Divergent Mechanisms of Interaction of Helicobacter pylori and Campylobacter jejuni with Mucus and Mucins

Abstract

f Helicobacter pylori and Campylobacter jejuni colonize the stomach and intestinal mucus, respectively. Using a combination of mucus-secreting cells, purified mucins, and a novel mucin microarray platform, we examined the interactions of these two organisms with mucus and mucins. H. pylori and C. jejuni bound to distinctly different mucins. C. jejuni displayed a striking tropism for chicken gastrointestinal mucins compared to mucins from other animals and preferentially bound mucins from specific avian intestinal sites (in order of descending preference: the large intestine, proximal small intestine, and cecum). H. pylori bound to a number of animal mucins, including porcine stomach mucin, but with less avidity than that of C. jejuni for chicken mucin. The strengths of interaction of various wild-type strains of H. pylori with different animal mucins were comparable, even though they did not all express the same adhesins. The production of mucus by HT29-MTX-E12 cells promoted higher levels of infection by C. jejuni and H. pylori than those for the non-mucus-producing parental cell lines. Both C. jejuni and H. pylori bound to HT29-MTX-E12 mucus, and while both organisms bound to glycosylated epitopes in the glycolipid fraction of the mucus, only C. jejuni bound to purified mucin. This study highlights the role of mucus in promoting bacterial infection and emphasizes the potential for even closely related bacteria to interact with mucus in different ways to establish successful infections.

Species identity dominates over environment in shaping the microbiota of small mammals

“…Of these mechanisms, those involving microbes binding to diverse host epitopes, such as immunoglobulins or mucus glycans, also have the potential to produce highly specific host‐microbe interactions (Schroeder & Cavacini ; Naughton et al . ), and generate species differences in the microbiota at a fine bacterial phylogenetic scale, as observed here. Our data also suggest diet may play a role generating species differences in the microbiota.…”

Use of Atomic Force Microscopy to Study the Multi-Modular Interaction of Bacterial Adhesins to Mucins

“…Methodologies to screen for bacterial adhesion to mucins have previously employed thin layer chromatography overlay [26], enzyme-linked immunosorbent assay [15], micro-titre plate assays [8,25,27], surface plasmon resonance [16,28,29,30,31], fluorescence spectroscopy [20], mucin microarrays [32], flow cytometry [33], and cell-based assays [26,34,35,36]. However, due to the complexity and diversity of mucin glycosylation, these methods typically provide qualitative binding data indicating only presence or absence of interaction.…”

Non-animal models of epithelial barriers (skin, intestine and lung) in research, industrial applications and regulatory toxicology

“…Currently, a clear limitation in studying human pathogens is the availability of relevant humanized infection models. This is particularly true for obligate human pathogens (e.g., Salmonella, Helicobacter pylori and Campylobacter jejuni) for which no animal reservoir is known (Dostal et al, 2014;Höner zu Bentrup et al, 2006;Naughton et al, 2013). Since simple cell culture systems and also animals are highly artificial models for obligate human pathogens, novel human infection models based on engineered human tissue are needed and are in fact currently under development (unpublished data).…”