Induction of ulceration and severe gastritis in Mongolian gerbil by Helicobacter pylori infection

Matsumoto, Satoru; Washizuka, Yukari; Matsumoto, Yoshimi; Tawara, Shuichi; Ikeda, Fumiaki; Yokota, Yoshiko; Karita, Mikio

doi:10.1099/00222615-46-5-391

Cited by 91 publications

(62 citation statements)

References 21 publications

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“…H. pylori has flagellar motility and is able to move through the Matsumoto et al, 1997;Yokota et al, 1991). The aim of this study is to investigate the effects of a defined luxS mutation on the characteristics of H. pylori and to determine whether the absence of AI-2 production allows H. pylori to infect and/or maintain infection in the gerbil gastric mucosa.…”

Section: Introductionmentioning

confidence: 99%

“…The Mongolian gerbil model, in which H. pylori is able to colonize long-term, is particularly easy to handle, and is useful as a small-animal model for the severe inflammation and obvious ulceration caused by H. pylori (Hirayama et al, 1996;Matsumoto et al, 1997;Yokota et al, 1991). The aim of this study is to investigate the effects of a defined luxS mutation on the characteristics of H. pylori and to determine whether the absence of AI-2 production allows H. pylori to infect and/or maintain infection in the gerbil gastric mucosa.…”

Section: Introductionmentioning

confidence: 99%

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Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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Helicobacter pylori is associated with gastric disorders in humans and some experimental animals, and possesses the luxS/type 2 autoinducer (AI-2) system. The effects of a specific luxS mutation on the characteristics of H. pylori were examined. On 0?3 % agar medium, motility of H. pylori HPKY08 (luxS : : cat) was significantly lower than that of wild-type H. pylori TK1402. The luxS-complemented strain HPKY21 exhibited motility comparable to that of H. pylori TK1402. It was shown that the luxS/AI-2 system plays an important role in H. pylori motility. The luxS mutant exhibited a reduced infection rate relative to the wild-type parent strain TK1402 in a Mongolian gerbil model. At 3 months after oral inoculation, lower numbers of H. pylori were detected by semi-quantitative real-time reverse transcription PCR (qRT-PCR) in luxS " mutant-infected gerbils than in TK1402-infected gerbils. Gastric inflammation and increased antibody titre for H. pylori were observed in TK1402-infected gerbils only. INTRODUCTIONQuorum sensing (QS) is a cell-to-cell communication system that regulates bacterial phenotypes, including the expression of virulence factor genes. The signalling molecules are known as autoinducers (AIs), and when these molecules reach a critical threshold concentration within a bacterial population, a signal transduction cascade is triggered, and this forms the basis for alterations in gene expression (Fuqua et al., 1994). Many Gram-negative bacteria utilize N-acylhomoserine lactone molecules, AI-1, as signals, while Gram-positive bacteria actively export peptides as signalling molecules. There is a second signalling system involved in a wide range of bacterial species (Schauder et al., 2001), and this system is utilized by both Gram-positive and Gram-negative bacteria. The signalling molecule known as type 2 autoinducer (AI-2) is a furanosyl borate diester (Chen et al., 2002), and the enzyme responsible for its synthesis is encoded by the luxS gene (Surette & Bassler, 1999). The genomes of many bacterial species, notably Escherichia coli, Salmonella enterica serovar Typhimurium, Shigella flexneri, Proteus mirabilis, Vibrio cholerae, Vibrio vulnificus, Campylobacter jejuni, Porphyromonas gingivalis, Bacillus subtilis, Streptococcus pyogenes, Streptococcus mutans, Clostridium perfringens and Clostridium difficile, include luxS homologues. In several of these, luxS-related AI-2 signals are involved in bacterial characteristics such as biofilm formation (Balestrino et al., 2005;Blehert et al., 2003;Fong et al., 2001;Wen & Burne 2004), flagella and motility (Jeon et al., 2003;Schneider et al., 2002;Stroeher et al., 2003), type III secretion systems (Sperandio et al., 1999), toxin production (Ohtani et al., 2002) and virulence (Lyon et al., 2001; Parsonnet et al., 1991;Stroeher et al., 2003).Helicobacter pylori has been identified as the aetiological agent of chronic active gastritis, peptic ulcer disease (Blaser, 1992;Graham, 1989), gastric adenocarcinoma (Parsonnet et al., 1991) and mucosal-associated lymphoid t...

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Osaki¹,

Hanawa²,

Manzoku³

et al. 2006

Journal of Medical Microbiology

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“…isolated from animals, such as H. felis from cats and H. mustelae from ferrets, in various animal models [ 11, 121. However, in the last 2 years new models for studying H. pylori-induced type B gastritis have been developed in euthymic mice and rats, and Mongolian gerbils [5,[13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Severe Gastritis in Guinea-Pigs Infected with Helicobacter Pylori

Sturegård

Sjunnesson

et al. 1998

Journal of Medical Microbiology

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An appropriate animal model is essential to study Helicobacter pylori infection. The aim of this study was to investigate if H. pylori can colonise the guinea-pig stomach and whether the infection causes gastritis and a serological response similar to that observed in man. Guinea-pigs were infected either with fresh H. pylori isolates from human gastric biopsies or with a guinea-pig passaged strain. When the animals were killed, 3 and 7 weeks after inoculation, samples were taken for culture, histopathology and serology. H. pylori was cultured from 22 of 29 challenged animals. All culture-positive animals exhibited a specific immune response against H. pylori antigens in Western blotting and gastritis in histopathological examination. Antibody titres in enzyme immunoassay were elevated among animals challenged with H. pylori. The inflammatory response was graded as severe in most animals and consisted of both polymorphonuclear leucocytes and lymphocytes. Erosion of the gastric epithelium was found in infected animals. These results suggest that the guinea-pig is suitable for studying H. pyloriassociated diseases. Moreover, guinea-pigs are probably more similar to man than any other small laboratory animal as regards gastric anatomy and physiology.

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“…In an effort to develop a model that would parallel as closely as possible the course of the infection as it occurs in the human host, Hirayama et al, 6 Matsumoto et al, 7 and Takahashi et al 8 inoculated a human strain of H. pylori into the stomach of Mongolian gerbils. After a short period most H. pylori-infected Mongolian gerbils developed chronic active gastritis.…”

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confidence: 99%

Helicobacter pylori-Induced Chronic Active Gastritis, Intestinal Metaplasia, and Gastric Ulcer in Mongolian Gerbils

Ikeno

Ota

Sugiyama

et al. 1999

The American Journal of Pathology

151

116

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Induction of ulceration and severe gastritis in Mongolian gerbil by Helicobacter pylori infection

Cited by 91 publications

References 21 publications

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Mutation of luxS affects motility and infectivity of Helicobacter pylori in gastric mucosa of a Mongolian gerbil model

Severe Gastritis in Guinea-Pigs Infected with Helicobacter Pylori

Helicobacter pylori-Induced Chronic Active Gastritis, Intestinal Metaplasia, and Gastric Ulcer in Mongolian Gerbils

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