The importance of local acid production in the distribution of Helicobacter felis in the mouse stomach

Danon, Stephen J.; O’Rourke, Jani; Moss, Nathan D.; Lee, Adrian V.

doi:10.1016/0016-5085(95)90686-x

Cited by 82 publications

(52 citation statements)

References 38 publications

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“…However, the site-dependent colonisation observed was similar to that described for man [34]. It has been reported that differences in distribution relate to differences in local acid output in the H. felis-infected mouse model [35]. This difference may be related to the acid output in 5-day-old and 2-week-old miniature pigs, which is lower than that in their 3-month-old cohorts.…”

Section: Discussionsupporting

confidence: 72%

Experimental Helicobacter pylori gastric infection in miniature pigs

Koga¹,

Shimada²,

Satô³

et al. 2002

Journal of Medical Microbiology

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An experimental Helicobacter pylori infection in miniature pigs was developed and investigated. Eighteen miniature pigs were inoculated with an H. pylori strain that has high virulence in mice at c. 5 3 10 10 cfu. H. pylori infection in miniature pigs was achieved by the administration of agar 1% in brucella broth with fetal bovine serum 10% just before inoculation. The bacterial colonisation and distribution were analysed by mapping of viable cell counts in the stomach in pigs of three different ages. The mapping assay was achieved on post-infection day 3 for the 5-day-old and 2-week-old pigs, and between days 41 and 43 for 3-month-old pigs. The highest cell counts were observed in 5-day-old pigs, which averaged 4:9 3 10 6 cfu=g of mucosa (n 4). The bacteria were colonised mainly in the cardiac and fundus gland region in the 5-day-old and 2-week-old pigs, whereas the colonisation sites did not depend on the region in the 3-month-old pigs. Biopsy assay of the antral mucosa of a 3-month-old pig after H. pylori infection showed that this infection persisted for >22 months. Serum antibody against H. pylori was detected in the infected pigs but not in the uninfected animal. Immunostaining demonstrated the presence of bacteria on the epithelial surface of the infected pigs. A microscopic ®nding common to all the infected pigs, focal gastritis with in®ltration of lymphocytes detected on the lesser curvature of the stomach, resembled the microscopic appearance in H. pylori-infected human patients. These results suggest that miniature pigs might be a suitable model for studying H. pylori infection.

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Section: Discussionsupporting

confidence: 72%

Experimental Helicobacter pylori gastric infection in miniature pigs

Koga¹,

Shimada²,

Satô³

et al. 2002

Journal of Medical Microbiology

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“…These data confirm that, as in humans, omeprazole monotherapy does not cure H. pylori infection in mice (28,29). This shift was seen in our early H. felis mouse model studies and is due to subtle changes in the local acid environment (8,25).…”

Section: Vol 47 2003 H Pylori Treatment Failures and The Transitiosupporting

confidence: 76%

Gastric Transitional Zones, Areas whereHelicobacterTreatment Fails: Results of a Treatment Trial Using the Sydney Strain Mouse Model

Zanten

Kolesnikow

Leung

et al. 2003

Antimicrob Agents Chemother

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Current combination therapies cure Helicobacter pylori infection in 75 to 85% of cases. However, many treatment failures are not explained by antibiotic resistance. Our goal was to explore treatment failures under in vivo conditions by using the H. pylori Sydney strain (SS1) mouse model. Mice infected with H. pylori (SS1) were treated with monotherapies or combination therapies used in human trials. Bacterial levels and distribution of organisms within the stomach were assessed 24 h after treatment to determine clearance and location of treatment failures and 29 days after treatment to determine cure rates. Except for treatment with metronidazole, mono-and dual therapies did not cure infection but resulted in decreases in bacterial levels and differences in distribution within the stomach. In cases of treatment failure when clarithromycin was used, omeprazole and dual therapy with omeprazole and amoxicillin resulted in organisms being cleared from the antrum, but organisms remained in the antrum-body transitional zone. The triple therapies of OMC and bismuth subcitrate, metronidazole, and tetracycline were successful in eradicating infection. Except for metronidazole monotherapy and triple therapy with OAC, there was good correlation between the Sydney strain mouse model and humans with respect to the success of antimicrobial therapy. The antrum-body transitional zone was identified as a sanctuary site in treatment failure. This could result from antimicrobial agents not functioning effectively at this site or bacteria in this location expressing products that protect them against antimicrobial agents. This is the first demonstration of a possible sanctuary site as a reason for failure of therapy.

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“…In contrast SS2000-infected BALB/c mice showed increased accumulation of mucosa-associated lymphoid tissue compared to those infected with SS1. This improved comparative model of H. pyloriinduced disease allowed dissection of both host and strain effects and thus will prove useful in further studies.Mouse models of Helicobacter pylori-induced disease have been extensively used in Helicobacter research and have been particularly useful in the elucidation of factors required for colonization, distribution and persistence of infection (10,29,31), the contribution of various virulence factors (some examples are given in references 12 and 43), and the development of vaccines (reviewed in reference 28). Early mouse model infection studies utilized Helicobacter felis, a close relative of H. pylori, because no H. pylori strains persistently colonized mice (5, 29).…”

mentioning

confidence: 99%

ChronicHelicobacter pyloriInfection with Sydney Strain 1 and a Newly Identified Mouse-Adapted Strain (Sydney Strain 2000) in C57BL/6 and BALB/c Mice

et al. 2004

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The mouse model of Helicobacter pylori-induced disease using Sydney strain 1 (SS1) has been used extensively in Helicobacter research. Herein we describe the isolation and characterization of a new mouse-colonizing strain for use in comparative studies. One strain capable of persistent mouse colonization was isolated from a total of 110 clinical isolates and is named here SS2000 (Sydney strain 2000). Genome typing revealed a number of differences between SS1 and SS2000 as well as between them and the respective original clinical isolates. In particular, SS2000 lacked the entire cag pathogenicity island, while SS1 contained all 27 genes of the island. C57BL/6 and BALB/c mice were infected with SS1 or SS2000 or were treated with broth medium (controls). After 6 months host-specific effects were evident, including lower colonization levels in the BALB/c animals. Few pathological differences were observed between SS1-and SS2000-infected animals. However, by 15 months postinfection, SS1-infected C57BL/6 mice had developed more severe gastritis than the SS2000-infected animals. In contrast SS2000-infected BALB/c mice showed increased accumulation of mucosa-associated lymphoid tissue compared to those infected with SS1. This improved comparative model of H. pyloriinduced disease allowed dissection of both host and strain effects and thus will prove useful in further studies.Mouse models of Helicobacter pylori-induced disease have been extensively used in Helicobacter research and have been particularly useful in the elucidation of factors required for colonization, distribution and persistence of infection (10,29,31), the contribution of various virulence factors (some examples are given in references 12 and 43), and the development of vaccines (reviewed in reference 28). Early mouse model infection studies utilized Helicobacter felis, a close relative of H. pylori, because no H. pylori strains persistently colonized mice (5, 29). In 1997, Lee et al. isolated H. pylori Sydney strain 1 (SS1) by screening a number of clinical isolates for their ability to colonize mice using a novel technique where a number of strains were pooled and passaged from mouse to mouse. SS1 was found to consistently colonize multiple strains of mice to a high level and to establish infection that persisted over many months, thus providing an ideal opportunity to study the effects of chronic infection and host specificity in this small rodent model (31). The difficulty in finding additional H. pylori strains that persistently colonize mice has hindered studies of strainspecific effects on infection and immunity. Other groups have attempted to isolate new mouse-colonizing strains, but in most cases those strains utilized do not colonize efficiently and often do so only transiently (some examples are given in references 34, 39, and 47). The SS1 mouse model has provided important information regarding H. pylori-related disease, particularly with respect to colonization properties. However, given the lack of well-scrutinized and characterized mouse-...

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The importance of local acid production in the distribution of Helicobacter felis in the mouse stomach

Cited by 82 publications

References 38 publications

Experimental Helicobacter pylori gastric infection in miniature pigs

Experimental Helicobacter pylori gastric infection in miniature pigs

Gastric Transitional Zones, Areas whereHelicobacterTreatment Fails: Results of a Treatment Trial Using the Sydney Strain Mouse Model

ChronicHelicobacter pyloriInfection with Sydney Strain 1 and a Newly Identified Mouse-Adapted Strain (Sydney Strain 2000) in C57BL/6 and BALB/c Mice

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