Induction of gastric ulcer and intestinal metaplasia in Mongolian gerbils infected withHelicobacter pylori

Hirayama, Fumihiro; Takagi, Shiro; Kusuhara, Hidenobu; Iwao, Eiji; Yokoyama, Yoshito; Ikeda, Yoshifumi

doi:10.1007/bf02347631

Cited by 222 publications

(155 citation statements)

References 9 publications

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“…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%

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%

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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“…In other study, with Mongolian gerbils, it was demonstrated that the resulting pathological changes in gastric mucosa are similar to those in humans [139]. Some studies demonstrated that when the animals were infected with H. pylori together with a carcinogen (Nmethyl-N-nitrosourea or N-methyl-N-nitro-N-nitrosoguanidine), they developed gastric cancer (both diffuse and intestinal types) that were at significantly higher frequencies than animals receiving either H. pylori or the carcinogen alone [140][141][142].…”

Section: Trends In Helicobacter Pylori Infection 138mentioning

confidence: 58%

Molecular Epidemiology of Helicobacter pylori in Brazilian Patients with Early Gastric Cancer and a Review to Understand the Prognosis of the Disease

Röesler¹,

Zeitune²

2014

Trends in Helicobacter Pylori Infection

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“…Fujioka et al infected Japanese monkeys with H. pylori and then followed the animals for a prolonged period, detecting the occurrence of gastric mucosal atrophy (15). Hirayama et al reported the appearance of intestinal metaplasia in Mongolian gerbils at 6 months after infection with H. pylori (13). It has become evident from these results that persistent H. pylori infection can cause atrophy and intestinal metaplasia, even in animals.…”

Section: Progression Of Persistent H Pylori Infection To Atrophic Gamentioning

confidence: 99%

“…An experimental model of persistent H. pylori infection has been difficult to develop, except in humans. In recent years, however, such models have been successfully created in monkeys (9), miniature pigs (10), mice (ll, 12), Mongolian gerbils (13), and other animals. The finding that H. pylori infection is closely related to the onset of gastric mucosal lesions has been obtained, as in the case of humans (14).…”

Section: Progression Of Persistent H Pylori Infection To Atrophic Gamentioning

confidence: 99%

Helicobacter pylori infection and Gastric Cancer.

Asaka

2002

Intern. Med.

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According to several prospective controlled epidemiologic studies, the positive rate of H. pylori antibody was showen to be higher in the patients with gastric cancer than in the control group. Retrospective studies on the association between gastric cancer and H. pylori have been conducted in a large numberof subjects and the results can be classified broadly into two categories, i.e., findings affirming an association and others denying it. Research concerning the association between gastric cancer and H. pylori has achieved great progress over time, leading to the recognition of this relationship by the WHO. One of the greatest concerns is to ascertain whether the final outcome of H. pylori-induced gastritis may lead to gastric cancer. The onset of gastric cancer can be explained as being caused not only by H. pylori infection, but also by a combination of various factors such as food and the environment. However, the possibility that the occurrence of gastric cancer, like the recurrence of peptic ulcer, can be prevented by eradication of H. pylori has also been suggested. Further progress in clinical research is needed to resolve this issue. (Internal Medicine 41: 1-6, 2002)

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Induction of gastric ulcer and intestinal metaplasia in Mongolian gerbils infected withHelicobacter pylori

Cited by 222 publications

References 9 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

Molecular Epidemiology of Helicobacter pylori in Brazilian Patients with Early Gastric Cancer and a Review to Understand the Prognosis of the Disease

Helicobacter pylori infection and Gastric Cancer.

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