Gastric Lesions and Immune Responses caused by Long-term Infection with Helicobacter heilmannii in C57BL/6 Mice

Park, Jong Hwan; Seok, Seung Hyeok; Baek, Min Won; Lee, H. Y.; Kim, D. J.; Park, Jae Hak

doi:10.1016/j.jcpa.2008.04.005

Cited by 10 publications

(8 citation statements)

References 20 publications

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“…IgG1-, IgG2b-, and IgM-positive cells were rarely detected in the gastric mucosa of H. suis -infected and the control mice. 38 However, these findings differed from the results by Peterson et al , 35 who exhibited that the number of IgG- and IgM-positive cells was increased in gastric mucosa of BALB/c mice infected with H. heilmannii. In outbred Swiss mice infected with Helicobacter felis , increased numbers of gastric IgA- and IgG-positive cells were also observed, although the number of IgM-positive cells was not increased.…”

Section: Discussionmentioning

confidence: 63%

Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice

et al. 2012

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Neonatal Fc receptors for immunoglobulin (Ig)G (FcRn) assume a central role in regulating host IgG levels and IgG transport across polarized epithelial barriers. We have attempted to elucidate the contribution of FcRn in controlling Helicobacter infection in the stomach. C57BL/6J wild-type or FcRn−/− mice were infected with Helicobacter heilmannii, and gastric lesions, bacterial load and the levels of antigen-specific IgG in serum and gastric juice were analyzed. The elevated levels of anti-H. heimannii IgG in gastric juice were observed exclusively in wild-type mice but not in FcRn−/− mice. In contrast, an increase in lymphoid follicles and bacterial loads along with deeper gastric epithelium invasion were noted in FcRn−/− mice. C57BL/6J wild-type or FcRn−/− mice were also infected with Helicobacter pylori SS1, and the results of the bacterial load in stomachs of these mice and the anti-H. pylori IgG levels in serum and gastric juice were similar to those from H. heilmannii infection. Our data suggest that FcRn can be functionally expressed in the stomach, which is involved in transcytosis of IgG, and prevent colonization by H. heilmannii and the associated pathological consequences of infection.

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Section: Discussionmentioning

confidence: 63%

Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice

et al. 2012

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“…1), whereas in the previous reports, the inoculation with gastric mucosal homogenates containing H. suis TKY induced gastric MALT lymphoma in a relatively short-term evaluation of a mouse model [25][26][27][28]. In addition, the infection with H. suis strains isolated from pigs caused gastric disorders in mice [49,50] and Mongolian gerbils [50]. To determine the difference in virulence among H. suis strains, further comparative genome analyses in addition to infection experiments will be needed.…”

Section: Discussionmentioning

confidence: 97%

Development of New PCR Primers by Comparative Genomics for the Detection of Helicobacter suis in Gastric Biopsy Specimens

et al. 2014

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“…This can be partly explained by the inability to perform immunological analysis; for example a recall assay using splenocytes and the recombinant protein, because the genome sequence of H. suis had not been examined until very recently. Park et al (2008) reported that the mRNA expression levels of IFN‐γ and IL‐10 in the gastric mucosa were enhanced in ‘ H. heilmannii ’‐infected mice, suggesting that both the Th1 and Th2 responses play roles in the gastric inflammatory responses induced by H. heilmannii '. In our study, the IFN‐γ mRNA expression level was significantly higher in the H. suis‐ infected C57BL/6J WT mice than in the noninfected mice at 12 weeks after infection (Fig.…”

Section: Discussionmentioning

confidence: 99%

IFN-γ plays an essential role in the pathogenesis of gastric lymphoid follicles formation caused byHelicobacter suisinfection

Mimura¹,

Yoshida²,

Nishiumi³

et al. 2011

FEMS Immunol Med Microbiol

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In this study, we aimed to assess the role of helper T cells in the development of gastric lymphoid follicles induced by Helicobacter suis infection. C57BL/6J mice were orally inoculated with H. suis. Six weeks after infection, gastric lymphoid follicles were observed in the gastric mucosa by hematoxylin and eosin staining, and the number of follicles was increased throughout the infection period. An immunohistological examination showed that the lymphoid follicles were composed of B cells, CD4-positive helper T cells, and dendritic cells (DC). It was also revealed that the mRNA expression level of interferon-γ (IFN-γ) in the gastric mucosa was significantly increased at 12 weeks after infection. No gastric lymphoid follicles were detected in IFN-γ-deficient mice that had been infected with H. suis at 12 weeks after infection, although the development of lymphoid follicles in IL-4-deficient mice infected with H. suis was similar to that seen in the wild-type mice. In conclusion, IFN-γ, a Th1 cytokine, is deeply involved in the pathogenesis of gastric lymphoid follicles induced by H. suis infection, and it is suggested that CD4-positive T cells and DC aid in the expansion of gastric lymphoid follicles.

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Gastric Lesions and Immune Responses caused by Long-term Infection with Helicobacter heilmannii in C57BL/6 Mice

Cited by 10 publications

References 20 publications

Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice

Neonatal Fc receptor for IgG (FcRn) expressed in the gastric epithelium regulates bacterial infection in mice

Development of New PCR Primers by Comparative Genomics for the Detection of Helicobacter suis in Gastric Biopsy Specimens

IFN-γ plays an essential role in the pathogenesis of gastric lymphoid follicles formation caused byHelicobacter suisinfection

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