Colonization and Tissue Tropism of <i>Helicobacter pylori</i> and a Novel Urease‐Negative <i>Helicobacter</i> Species in ICR Mice Are Independent of Route of Exposure

McCathey, Sonya N.; Shomer, Nirah H.; Schrenzel, Mark D.; Whary, Mark T.; Taylor, Nancy S.; Fox, James G.

doi:10.1046/j.1523-5378.1999.99291.x

Cited by 7 publications

(8 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similarly, serum IgG levels were high in Swiss Webster outbred mice dosed intraperitoneally with H. pylori, even though only a minority (one out of eight) of the mice was colonized with H. pylori 1 month after dosing. The serum titres were considerably greater than antibody titres measured in orally dosed mice (McCathey et al, 1999). In mice dosed intraperitoneally with an enteric helicobacter, the organism was not isolated from various tissues (blood, lung, spleen, liver and kidneys) 30 days p.i., but was cultured from faeces (McCathey et al, 1999).…”

Section: Discussionmentioning

confidence: 73%

“…The bacterial pellet was resuspended in sterile PBS to a concentration of approximately 10 7 organisms ml 21 based on spectrophotometric examination. Using a previously published inoculation strategy, experimental mice (24 males, 24 females) received 0.2 ml inoculum by intraperitoneal injection, whilst control mice (8 males, 8 females) were given 0.2 ml sterile PBS (McCathey et al, 1999;Shomer et al, 2001). One mouse from each cage (total of two control and six experimental mice of each sex) was necropsied at 6 and 12 months after dosing; necropsies on the remaining mice were performed when the study was concluded at 18 months postinoculation (p.i.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Experimental Helicobacter marmotae infection in A/J mice causes enterohepatic disease

Patterson

Rogers

Fox

2010

Journal of Medical Microbiology

Self Cite

View full text Add to dashboard Cite

Helicobacter marmotae has been identified in the inflamed livers of Eastern woodchucks (Marmota monax) infected with woodchuck hepatitis virus (WHV), as well as from the livers of WHV-negative woodchucks. Because the majority of WHV-positive woodchucks with hepatic tumours were culture or PCR positive for this helicobacter, and WHV-negative woodchucks with H. marmotae had hepatitis, the bacterium may have a role in tumour promotion related to chronic inflammation. In this study, the type strain of H. marmotae was inoculated intraperitoneally into 48 male and female A/J mice, a strain noted to be susceptible to Helicobacter hepaticus-induced liver tumours. Sixteen mice served as mock-dosed controls. At 6, 12 and 18 months post-inoculation (p.i.), there were statistically significant (P<0.05) differences in mean inflammation scores for the caecum and proximal colon between experimentally infected and control mice. Differences in hepatic inflammation were significant (P<0.05) at 6 and 12 months p.i. between the two groups but not at the 18 month time point. Two infected male mice had livers with severe hepatitis, and the liver samples were culture positive for H. marmotae. Serum IgG levels in the mice dosed with H. marmotae were elevated for the duration of the study. These results demonstrate that the woodchuck helicobacter can successfully colonize mice and cause enterohepatic disease. In the future, a mouse-adapted strain of H. marmotae could be selected to maximize colonization and lesion development. Such a woodchuck helicobacter-infected mouse model could be used to dissect potential mechanisms of microbial co-carcinogenesis involved in tumour development in woodchucks with WHV and in humans with hepatitis B virus.

show abstract

Section: Discussionmentioning

confidence: 73%

Section: Methodsmentioning

confidence: 99%

Experimental Helicobacter marmotae infection in A/J mice causes enterohepatic disease

Patterson

Rogers

Fox

2010

Journal of Medical Microbiology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Studies have shown that mice inoculated intraperitoneally with H. pylori develop acute hepatitis [21]. We established the mouse model of H. pylori infection by inoculating orally instead of intraperitoneally, as the usual route of H. pylori infection is faecal-oral.…”

Section: Discussionmentioning

confidence: 99%

The pathological effect of Helicobacter pylori infection on liver tissues in mice

Huang

Tian

Fan

et al. 2009

Clinical Microbiology and Infection

View full text Add to dashboard Cite

Helicobacter pylori infection is associated with chronic gastritis, peptic ulcer, gastric adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Some reports also suggest that it causes extragastric disease, including hepatitis. In this study, the pathological changes in the liver and gall bladder in H. pylori-colonized C57BL/6 mice were investigated. Twenty mice were inoculated orally with H. pylori strain SS1, and ten controls were injected with phosphate-buffered saline. Gastric colonization with H. pylori was assessed at 2 months after inoculation. Mice were examined at 8 months by histopathology, culture for H. pylori, and PCR for specific H. pylori genes. All C57BL/6 mice infected with H. pylori for 8 months developed severe gastric mucosal inflammation. Three mice showed mild-to-moderate multifocal hepatitis. The gall bladder mucosa of one H. pylori-infected mouse showed thickening of the mucous membrane with mild submucosal lymphocytic infiltration. H. pylori was observed morphologically in four liver specimens and six gall bladders from infected mice by immunohistochemistry. Specific H. pylori genes were also detected in six liver samples from infected mice, six samples of bile, and two blood samples by nested PCR. Thus, H. pylori inoculated orally may reach the hepatobiliary system and cause inflammation as an independent aetiological factor. The pathway to the liver may be via the blood or the biliary system.

show abstract

“…We confirmed this by the presence of chronic inflammation in the livers of ip-treated mothers but not ig-treated mothers. In a study with H. pylori and a novel Helicobacter species, McCathey et al (1999) found that ip-administered bacteria, but not ig administration at the same titer, resulted in hepatitis and elicited a much greater immune response. Thus, the likelihood of transmission of progressive disease to offspring may be a function of degree of infection of the mother, and the very high incidences of hepatitis and tumors in male offspring of naturally infected mothers, seen in our original population of infected mice, may reflect the level of bacterial burden accumulated over generations.…”

Section: Discussionmentioning

confidence: 99%

Marked Liver Tumorigenesis by Helicobacter hepaticus Requires Perinatal Exposure

Diwan

Sipowicz

Logsdon

et al. 2008

Environ Health Perspect

View full text Add to dashboard Cite

BackgroundAlthough severe hepatitis and liver tumors occur in a high percentage of A/J male mice naturally infected with Helicobacter hepaticus, these effects have not been observed after injection of adult mice with the bacteria.ObjectivesWe tested the hypothesis that perinatal exposure to the bacteria is required for liver tumorigenesis.MethodsA/J female mice were infected by intragastric (ig) or intraperitoneal (ip) treatment with 1.5 × 108 H. hepaticus before pregnancy. We examined offspring at progressive time intervals, including some kept until natural death in old age. A/J, BALB/c, and C57BL/6 weanling male mice were similarly treated ig with the bacteria and observed for up to 2 years.ResultsAfter ip bacterial infection of A/J females, 41% of their male offspring developed hepatitis and 33% had hepatocellular tumors, including 18% with hepatocellular carcinoma. Treatment by the ig route resulted in a similar incidence of hepatitis in offspring (35%) but fewer total liver tumors (8%) and carcinomas (4%). By contrast, ig instillation of H. hepaticus in weanling A/J, C57BL/6, or BALB/c mice resulted in low incidence of hepatitis (0–20%) and few liver tumors, despite presence of bacteria confirmed in feces.ConclusionsResults indicate that a high incidence of liver tumors in mice infected with H. hepaticus requires perinatal exposure. Contributing perinatal factors could include known high sensitivity of neonatal liver to tumor initiation, and/or modulation of immune response to the bacterium or its toxins. Mechanisms of human perinatal sensitivity to such phenomena can be studied with this model.

show abstract

Colonization and Tissue Tropism of Helicobacter pylori and a Novel Urease‐Negative Helicobacter Species in ICR Mice Are Independent of Route of Exposure

Cited by 7 publications

References 42 publications

Experimental Helicobacter marmotae infection in A/J mice causes enterohepatic disease

Experimental Helicobacter marmotae infection in A/J mice causes enterohepatic disease

The pathological effect of Helicobacter pylori infection on liver tissues in mice

Marked Liver Tumorigenesis by Helicobacter hepaticus Requires Perinatal Exposure

Contact Info

Product

Resources

About