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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).
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.
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author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
IMMUNE-RESPONSE, C57BL/6 MICE, PYLORI INFECTION, LONG-TERM INFECTION, INFLAMMATORY RESPONSE, LYMPHOID-TISSUE, MALT LYMPHOMA, FELIS INFECTION, HEILMANNII INFECTION, MUCOSA
journal title
PLOS ONE
PLoS One
volume
5
issue
11
article_number
e14083
pages
11 pages
Web of Science type
Article
Web of Science id
000284467200014
JCR category
BIOLOGY
JCR impact factor
4.411 (2010)
JCR rank
12/84 (2010)
JCR quartile
1 (2010)
ISSN
1932-6203
DOI
10.1371/journal.pone.0014083
language
English
UGent publication?
yes
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
1217271
handle
http://hdl.handle.net/1854/LU-1217271
date created
2011-05-05 09:54:38
date last changed
2011-05-06 16:14:04
@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},
}

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.