Abstract
Background“Helicobacter (H.) heilmannii” type 1 is the most prevalent gastric non-H. pylori Helicobacter species in humans suffering from gastric disease. It has been shown to be identical to H. suis, a bacterium which is mainly associated with pigs. To obtain better insights into the long-term pathogenesis of infections with this micro-organism, experimental infections were carried out in different rodent models.Methodology/Principal FindingsMongolian gerbils and mice of two strains (BALB/c and C57BL/6) were infected with H. suis and sacrificed at 3 weeks, 9 weeks and 8 months after infection. Gastric tissue samples were collected for PCR analysis, histological and ultrastructural examination. In gerbils, bacteria mainly colonized the antrum and a narrow zone in the fundus near the forestomach/stomach transition zone. In both mice strains, bacteria colonized the entire glandular stomach. Colonization with H. suis was associated with necrosis of parietal cells in all three animal strains. From 9 weeks after infection onwards, an increased proliferation rate of mucosal epithelial cells was detected in the stomach regions colonized with H. suis. Most gerbils showed a marked lymphocytic infiltration in the antrum and in the forestomach/stomach transition zone, becoming more pronounced in the course of time. At 8 months post infection, severe destruction of the normal antral architecture at the inflamed sites and development of mucosa-associated lymphoid tissue (MALT) lymphoma-like lesions were observed in some gerbils. In mice, the inflammatory response was less pronounced than in gerbils, consisting mainly of mononuclear cell infiltration and being most severe in the fundus.Conclusions/Significance H. suis causes death of parietal cells, epithelial cell hyperproliferation and severe inflammation in mice and Mongolian gerbil models of human gastric disease. Moreover, MALT lymphoma-like lesions were induced in H. suis-infected Mongolian gerbils. Therefore, the possible involvement of this micro-organism in human gastric disease should not be neglected.
Highlights
Several infection studies have been performed in mice with ‘‘H. heilmannii’’ or ‘‘tightly coiled spiral bacteria’’, often without a clear identification of infection with Helicobacter (H.) pylori is considered to be the major cause of gastritis, peptic ulcer disease [1,2], gastric adenocarcinoma [3] and mucosa-associated lymphoid tissue (MALT) lymphoma [4] in humans, these gastric diseases have been associated with other helicobacters, nowadays referred to as gastric non-H. pylori Helicobacter (NHPH) species or ‘‘H
In Mongolian gerbils, long-term infection with H. suis was associated with severe gastric pathology, including necrosis of gastric epithelial cells and the development of gastric MALT lymphoma-like lesions
At 3 and 9 weeks post infection, increased numbers of mature macrophages were observed in the gastric mucosa of H. suis infected mice, mainly in the BALB/c strain
Summary
Infection with Helicobacter (H.) pylori is considered to be the major cause of gastritis, peptic ulcer disease [1,2], gastric adenocarcinoma [3] and mucosa-associated lymphoid tissue (MALT) lymphoma [4] in humans, these gastric diseases have been associated with other helicobacters, nowadays referred to as gastric non-H. pylori Helicobacter (NHPH) species or ‘‘H.heilmannii’’ [5,6,7,8]. Mucus or homogenized gastric tissue of infected mice, pigs or non-human primates was always used as inoculum [15,16,17,18,19,20,21,22]. This implies that other micro-organisms were inoculated along with the helicobacters, which might influence the results, as has been shown for gastric yeasts interfering with a gastric H. suis infection in Mongolian gerbils [23]. In Mongolian gerbils, long-term infection with H. suis was associated with severe gastric pathology, including necrosis of gastric epithelial cells and the development of gastric MALT lymphoma-like lesions
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