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Helicobacter suis causes severe gastric pathology in mouse and Mongolian gerbil models of human gastric disease

Bram Flahou (UGent) , Freddy Haesebrouck (UGent) , Frank Pasmans (UGent) , Katharina D'Herde (UGent) , Ann Driessen, Kim Van Deun (UGent) , Annemieke Smet (UGent) , Luc Duchateau (UGent) , Koen Chiers (UGent) and Richard Ducatelle (UGent)
(2010) PLOS ONE. 5(11).
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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 findings: Mongolian 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.
Keywords
IMMUNE-RESPONSE, C57BL/6 MICE, PYLORI INFECTION, LONG-TERM INFECTION, INFLAMMATORY RESPONSE, LYMPHOID-TISSUE, MALT LYMPHOMA, FELIS INFECTION, HEILMANNII INFECTION, MUCOSA

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Chicago
Flahou, Bram, Freddy Haesebrouck, Frank Pasmans, Katharina D’Herde, Ann Driessen, Kim Van Deun, Annemieke Smet, Luc Duchateau, Koen Chiers, and Richard Ducatelle. 2010. “Helicobacter Suis Causes Severe Gastric Pathology in Mouse and Mongolian Gerbil Models of Human Gastric Disease.” Plos One 5 (11).
APA
Flahou, B., Haesebrouck, F., Pasmans, F., D’Herde, K., Driessen, A., Van Deun, K., Smet, A., et al. (2010). Helicobacter suis causes severe gastric pathology in mouse and Mongolian gerbil models of human gastric disease. PLOS ONE, 5(11).
Vancouver
1.
Flahou B, Haesebrouck F, Pasmans F, D’Herde K, Driessen A, Van Deun K, et al. Helicobacter suis causes severe gastric pathology in mouse and Mongolian gerbil models of human gastric disease. PLOS ONE. 2010;5(11).
MLA
Flahou, Bram, Freddy Haesebrouck, Frank Pasmans, et al. “Helicobacter Suis Causes Severe Gastric Pathology in Mouse and Mongolian Gerbil Models of Human Gastric Disease.” PLOS ONE 5.11 (2010): n. pag. Print.
@article{1217271,
  abstract     = {Background: {\textquotedblleft}Helicobacter (H.) heilmannii{\textquotedblright} 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 findings: Mongolian 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.},
  articleno    = {e14083},
  author       = {Flahou, Bram and Haesebrouck, Freddy and Pasmans, Frank and D'Herde, Katharina and Driessen, Ann and Van Deun, Kim and Smet, Annemieke and Duchateau, Luc and Chiers, Koen and Ducatelle, Richard},
  issn         = {1932-6203},
  journal      = {PLOS ONE},
  keyword      = {IMMUNE-RESPONSE,C57BL/6 MICE,PYLORI INFECTION,LONG-TERM INFECTION,INFLAMMATORY RESPONSE,LYMPHOID-TISSUE,MALT LYMPHOMA,FELIS INFECTION,HEILMANNII INFECTION,MUCOSA},
  language     = {eng},
  number       = {11},
  pages        = {11},
  title        = {Helicobacter suis causes severe gastric pathology in mouse and Mongolian gerbil models of human gastric disease},
  url          = {http://dx.doi.org/10.1371/journal.pone.0014083},
  volume       = {5},
  year         = {2010},
}

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