Abstract
Helicobacter pylori colonization is highly prevalent among humans and causes significant gastric disease in a subset of those infected. When present, this bacterium dominates the gastric microbiota of humans and induces antimicrobial responses in the host. Since the microbial context of H. pylori colonization influences the disease outcome in a mouse model, we sought to assess the impact of H. pylori challenge upon the pre-existing gastric microbial community members in the rhesus macaque model. Deep sequencing of the bacterial 16S rRNA gene identified a community profile of 221 phylotypes that was distinct from that of the rhesus macaque distal gut and mouth, although there were taxa in common. High proportions of both H. pylori and H. suis were observed in the post-challenge libraries, but at a given time, only one Helicobacter species was dominant. However, the relative abundance of non-Helicobacter taxa was not significantly different before and after challenge with H. pylori. These results suggest that while different gastric species may show competitive exclusion in the gastric niche, the rhesus gastric microbial community is largely stable despite immune and physiological changes due to H. pylori infection.
Highlights
Helicobacter pylori is a bacterium that colonizes the stomach of approximately half of the world’s human population, in socioeconomically-challenged regions around the globe
H. pylori infection has been associated with distinct gastric microbial community structures [5], which may in part determine the outcome of H. pylori infection
In the INS-GAS mouse model of gastric cancer, germ-free mice infected with H. pylori experienced significantly less disease and delayed onset of neoplasia compared to those colonized with conventional microbiota [6]
Summary
Helicobacter pylori is a bacterium that colonizes the stomach of approximately half of the world’s human population, in socioeconomically-challenged regions around the globe. In a minority of those infected, H. pylori can cause peptic ulcers (10– 20%), gastric cancer (1–2%), and rarely mucosa-associated lymphoid tissue (MALT) lymphoma [1]. It is a welladapted and highly abundant resident of the gastric environment if present, H. pylori is not alone [2]. The mechanisms by which H. pylori infection may impact other gastric microbiota are not well understood, but could include induction of host antimicrobial peptides, such as b-defensin 2, elafin, siderocalin, and other innate immune effects [8], or by direct killing of other bacteria through the activity of its own cecropin-like peptide [9]. H. pylori induces physiological changes in the host stomach, including alterations in pH [10], epithelial surface [11], gastric hormones [12], and immunologic state [13], all of which may alter the composition of the gastric microbiome
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