Severe Gastritis in Guinea-Pigs Infected with Helicobacter Pylori

Sturegård, Erik; Sjunnesson, Håkan; Ho, Bow; Wïllén, Roger; Aleljung, Pär; Ng, Han Chong; Wadström, Torkel

doi:10.1099/00222615-47-12-1123

Cited by 36 publications

(52 citation statements)

References 23 publications

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“…A Mongolian gerbil model was recently optimised to study the gastric in¯ammation response to H. pylori infection with a strong induction of pro-and anti- oxidants [28]. Also, a guinea-pig model has been developed for experimental H. pylori infection yielding a strong gastric in¯ammation response [29]. These animal models may now be used to evaluate various candidates for a non-antibiotic treatment strategy to combat H. pylori infections.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Helicobacter pylori infection by bovine milk glycoconjugates in a BALB/cA mouse model

Wang¹,

Hirmo²,

Wïllén

et al. 2001

Journal of Medical Microbiology

103

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The attachment of Helicobacter pylori to the human gastric mucosa is a complex process involving several speci®c structures recognised by the cell surface receptors. Sialylated multivalent high mol. wt glycoproteins have been shown to inhibit H. pylori sialic acidspeci®c haemagglutination. This study explored whether sialylated glycoconjugates from bovine milk could inhibit an experimental H. pylori infection in a mouse model. BALB=cA mice (6±8 weeks old) were inoculated with a mouse-passaged H. pylori strain 317p. Four weeks after infection the mice were given lactoferrin (iron-free LF or 20% iron-saturated LF) or bovine milk fat globule membrane fractions (MFGM or defatted MFGM) orally (400 mg=kg body weight) once daily for 10 days and then killed to examine for bacterial colonisation and gastritis. Mice treated with iron-free LF, 20% iron-saturated LF, MFGM or defatted MFGM showed 30%, 10%, 20% or 20% healing rates, respectively, when compared with the H. pylori-infected control. Gastric colonisation by H. pylori was remarkably decreased in all mice treated with bovine milk glycoconjugates and the in¯ammation score was also signi®cantly lower in treated mice than in infected control animals. The fact that there was no signi®cant difference between iron-free LF and iron-saturated LF or MFGM and defatted MFGM suggested that iron is not crucial for inhibition of H. pylori by lactoferrin and that the lipid part of MFGM is not important for anti-H. pylori activity. In conclusion, bovine milk glycoconjugates showed potencies to inhibit H. pylori infection in this mouse model and, therefore, could be considered as candidates for non-antibiotic strategies against H. pylori infection in man.

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Section: Discussionmentioning

confidence: 99%

Inhibition of Helicobacter pylori infection by bovine milk glycoconjugates in a BALB/cA mouse model

Wang¹,

Hirmo²,

Wïllén

et al. 2001

Journal of Medical Microbiology

103

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Section: Introductionmentioning

confidence: 99%

“…The guinea pig model for H. pylori infection has some attractive features, such as ease of husbandry and animal size. The guinea pig stomach has several features in common with the human stomach that are lacking in the mouse model, such as sterility and the production of IL8 (Shomer et al, 1998;Sturegard et al, 1998).In this study, we have employed the guinea pig model of H. pylori infection to characterize the role of the OMPs AlpA, AlpB, OipA and HopZ in colonization of the stomach by H. pylori. Isogenic mutants in the alpA, alpB, oipA and hopZ genes were created in the guinea pig-adapted H. pylori strain GP15 and used to infect guinea pigs with either single mutants or 1 : 1 mixtures of the wild-type strain and a single mutant.…”

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confidence: 99%

Role of the Helicobacter pylori outer-membrane proteins AlpA and AlpB in colonization of the guinea pig stomach

Jonge

Durrani

Rijpkema

et al. 2004

Journal of Medical Microbiology

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The human gastric pathogen Helicobacter pylori expresses several putative outer-membrane proteins (OMPs), but the role of individual OMPs in colonization of the stomach by H. pylori is still poorly understood. The role of four such OMPs (AlpA, AlpB, OipA and HopZ) in a guinea pig model of H. pylori infection has been investigated. Single alpA, alpB, hopZ and oipA isogenic mutants were constructed in the guinea pig-adapted, wild-type H. pylori strain GP15. Guinea pigs were inoculated intragastrically with the wild-type strain, single mutants or a mixture of the wild-type and a single mutant in a 1 : 1 ratio. Three weeks after infection, H. pylori could be isolated from stomach sections of all animals that were infected with the wild-type, the hopZ mutant or the oipA mutant, but from only five of nine (P ¼ 0 . 18) and one of seven (P ¼ 0 . 02) animals that were infected with the alpA or alpB mutants, respectively. The hopZ and oipA mutants colonized the majority of animals that were inoculated with the strain mixture, whereas alpA and alpB mutants could not be isolated from animals that were infected with the strain mixture (P , 0 . 01). Specific IgG antibody responses were observed in all animals that were infected with either the wild-type or a mutant, but IgG levels were lower in animals that were infected with either the alpA or the alpB mutants, compared to the wildtype strain (P , 0 . 05). In conclusion, absence of AlpA or AlpB is a serious disadvantage for colonization of the stomach by H. pylori. INTRODUCTIONThe human pathogen Helicobacter pylori persistently colonizes the gastric mucosa of more than half of the world's population. Colonization by H. pylori always results in active gastritis and is associated with the development of peptic ulcer disease, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (Kuipers, 1997). Several H. pylori factors are commonly believed to be required for efficient, lifelong colonization of the gastric mucosa, including urease activity (Eaton & Krakowka, 1994), motility by polar sheathed flagella (Eaton et al., 1996) and adherence to gastric epithelial cells (Hessey et al., 1990;Guruge et al., 1998;Yamaoka et al., 2002). Adherence to gastric epithelial cells protects H. pylori against peristalsis and mucosal shedding and warrants access to nutrients that are released from damaged epithelium.It appears that mucosal adhesion of H. pylori is associated directly with mucosal damage (Hessey et al., 1990;Guruge et al., 1998). Adhesion of H. pylori is mediated in part via specific adhesins, such as the sialyl Lewis x -binding protein SabA (Mahdavi et al., 2002) and the Lewis b blood group antigen-binding protein BabA (Boren et al., 1993;Ilver et al., 1998). However, the H. pylori genome also encodes several other outer-membrane proteins (OMPs) that have been associated with adhesion, including OipA, HopZ, AlpA and AlpB (Alm et al., 1999;Evans & Evans, 2000;Tomb et al., 1997). The role of these individual OMPs in adhesion of H. pylori is still relatively poorly un...

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“…The guinea pig model of H. pylori infection was first described in the late 1990s (565,600). The guinea pig model has advantages similar to the mouse model in ease of husbandry and animal size.…”

Section: Animal Modelsmentioning

confidence: 99%

Pathogenesis ofHelicobacter pyloriInfection

2006

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SUMMARY Helicobacter pylori is the first formally recognized bacterial carcinogen and is one of the most successful human pathogens, as over half of the world's population is colonized with this gram-negative bacterium. Unless treated, colonization usually persists lifelong. H. pylori infection represents a key factor in the etiology of various gastrointestinal diseases, ranging from chronic active gastritis without clinical symptoms to peptic ulceration, gastric adenocarcinoma, and gastric mucosa-associated lymphoid tissue lymphoma. Disease outcome is the result of the complex interplay between the host and the bacterium. Host immune gene polymorphisms and gastric acid secretion largely determine the bacterium's ability to colonize a specific gastric niche. Bacterial virulence factors such as the cytotoxin-associated gene pathogenicity island-encoded protein CagA and the vacuolating cytotoxin VacA aid in this colonization of the gastric mucosa and subsequently seem to modulate the host's immune system. This review focuses on the microbiological, clinical, immunological, and biochemical aspects of the pathogenesis of H. pylori.

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Severe Gastritis in Guinea-Pigs Infected with Helicobacter Pylori

Cited by 36 publications

References 23 publications

Inhibition of Helicobacter pylori infection by bovine milk glycoconjugates in a BALB/cA mouse model

Inhibition of Helicobacter pylori infection by bovine milk glycoconjugates in a BALB/cA mouse model

Role of the Helicobacter pylori outer-membrane proteins AlpA and AlpB in colonization of the guinea pig stomach

Pathogenesis ofHelicobacter pyloriInfection

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