Effect of Th1 cytokines on acid secretion in pharmacologically characterised mouse gastric glands

Padol, Ireneusz T.

doi:10.1136/gut.2003.026435

Cited by 29 publications

(20 citation statements)

References 43 publications

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“…5 Using mousespecific recombinant cytokines in an in vitro model of pharmacologically characterized gastric glands isolated from BALB/c and C57BL/6 mice, investigators convincingly demonstrated that only two (among IFN-␥, IL-2, IL-12, IL-4, IL-6, and IL-10) mouse cytokines, IL-2 and IFN-␥, had a direct, dose-dependent inhibitory effect on acid secretion. 46 These data are consistent with these two cytokines being elevated in a Th1 proinflammatory response due to gastric helicobacter infection, which over time develop gastric atrophy, dysplasia, and cancer. 19,47 In an H. felis C57BL mouse model, coinfection with a helminth significantly reduced IFN-␥, IL-1␤, and TNF-␣ mRNA and attenuated premalignant lesions.…”

Section: Fected Tff2supporting

confidence: 78%

Accelerated Progression of Gastritis to Dysplasia in the Pyloric Antrum of TFF2−/− C57BL6 × Sv129 Helicobacter pylori-Infected Mice

Fox

Rogers

Whary

et al. 2007

The American Journal of Pathology

118

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Trefoil factor family 2 (TFF2) is up-regulated inHelicobacter spp.-infected gastric tissues of both humans and mice. To ascertain the biological effects of TFF2 in vivo, TFF2 ؊/؊ C57BL/6 ؋ Sv129 and wild-type (WT) C57BL/6 ؋ Sv129 mice were orally infected with Helicobacter pylori SS1. Mice were evaluated for gastric H. pylori colonization, pathology, and cytokine profiles at 6 and 19 months post inoculation (pi). At 6 months pi, there was a significant difference (P < 0.05) for epithelial criteria (mucosal defects, atrophy, hyperplasia, pseudopyloric metaplasia, and dysplasia) in the corpus of TFF2 ؊/؊ versus WT mice. At 19 months pi, a similar statistical difference in epithelial parameters was noted in the antrum of TFF2 ؊/؊ versus WT mice (P < 0.01). All of the TFF2 ؊/؊ H. pyloriinfected mice had high-grade antral dysplasia, including gastric intraepithelial neoplasia, which was statistically significant (P < 0.05) compared with the infected WT mice. Levels of interferon-␥ were markedly elevated in the gastric mucosa of infected TFF2 ؊/؊ mice at both 6 and 19 months pi. TFF2 provided a cytoprotective and/or anti-inflammatory effect against the progression of premalignant lesions of the gastric corpus at 6 months pi and in the pyloric antrum in H. pylori-infected mice at 19 months pi. These data support a protective role for TFF2 in part by modulating levels of gastric interferon-␥ in the development of H. pylori-associated premalignancy of the distal stomach.

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Section: Fected Tff2supporting

confidence: 78%

Accelerated Progression of Gastritis to Dysplasia in the Pyloric Antrum of TFF2−/− C57BL6 × Sv129 Helicobacter pylori-Infected Mice

Fox

Rogers

Whary

et al. 2007

The American Journal of Pathology

118

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“…In a chronic restraint stress mice model, the inhibition of CD4+ CD25+ regulatory T cells by anti-CD25 antibodies induced a significant increase in plasma IL-2 [83]. Moreover, IL-2 is also thought to potentiate H. pylori-associated gastroduodenal disorders by controlling Th1 immune responses [84].…”

Section: Kotob Et Almentioning

confidence: 99%

Quercetin and Ellagic Acid in Gastric Ulcer Prevention: An Integrated Scheme of the Potential Mechanisms of Action From in Vivo Study

Kotob

Sayed

Mohamed

et al. 2018

Asian J Pharm Clin Res

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Objective: The present study was initiated to describe the gastroprotective role of quercetin (Qu) and ellagic acid (EA) on aspirin-induced gastric ulcer (GU) in rats.Methods: Forty adult female albino rats of Wistar strain were distributed into: Control group, GU group, Omeprazole group, Qu group, and EA group. Gross examination, biochemical analyses including serum adrenocorticotropic hormone (ACTH), serotonin (ST), ferritin, heme oxygenase-1 (HO-1), interleukin-2 (IL-2), advanced glycosylation end products (AGEs), and fibronectin (FN) levels were estimated. Moreover, histopathological and histochemical examinations of stomach tissue samples were carried out.Results: Gross examination of gastric mucosa of rats in GU group revealed hyperemia of the stomach mucosa. Furthermore, rats in GU group experienced a significant rise in serum ACTH, ferritin, HO-1, IL-2 and AGEs levels accompanied with significant drop in serum ST and FN levels versus control counterparts. Pre-treatment of GU group with Omeprazole, Qu or EA caused marked improvement in the measured biochemical parameters. Histopathological and histochemical examinations of stomach tissue samples documented the protective action of Omeprazole, Qu and EA with different degrees against GU caused by aspirin. Conclusion:As a conclusion to this study, we can state that both Qu and EA have gastroprotective effect against aspirin-induced GU in rat model. Of note, Qu showed superior impact than EA as an antiulcer agent in this study. The corresponding mechanisms are speculated to be associated with inhibiting stress-induced gastric lesion, attenuating the oxidative stress, iron chelation and blunting ferritin level, modulating inflammatory cascade, and promoting the healing process.

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“…The most common and detrimental immune response involves the Th1 pro-inflammatory cytokines, most prominently IFNγ from T cells, and IL-1β and TNFα from tissue or invading macrophages [5], [6], [7], [8], [9]. Indeed, pro-inflammatory cytokine IFNγ has been shown to contribute to the pathogenesis and development of gastric metaplasia [5], [9], [10] and cancer [10].…”

Section: Introductionmentioning

confidence: 99%

Sonic Hedgehog Mediates the Proliferation and Recruitment of Transformed Mesenchymal Stem Cells to the Stomach

et al. 2013

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Studies using Helicobacter-infected mice show that bone marrow-derived mesenchymal stem cells (MSCs) can repopulate the gastric epithelium and promote gastric cancer progression. Within the tumor microenvironment of the stomach, pro-inflammatory cytokine interferon-gamma (IFNγ) and Sonic hedgehog (Shh) are elevated. IFNγ is implicated in tumor proliferation via activation of the Shh signaling pathway in various tissues but whether a similar mechanism exists in the stomach is unknown. We tested the hypothesis that IFNγ drives MSC proliferation and recruitment, a response mediated by Shh signaling. The current study uses transplantation of an in vitro transformed mesenchymal stem cell line (stMSCvect), that over-expresses hedgehog signaling, in comparison to non-transformed wild-type MSCs (wtMSCs), wtMSCs transfected to over-express Shh (wtMSCShh), and stMSCs transduced with lentiviral constructs containing shRNA targeting the Shh gene (stMSCShhKO). The effect of IFNγ on MSC proliferation was assessed by cell cycle analysis in vitro using cells treated with recombinant IFNγ (rmIFNγ) alone, or in combination with anti-Shh 5E1 antibody, and in vivo using mice transplanted with MSCs treated with PBS or rmIFNγ. In vitro, IFNγ significantly increased MSC proliferation, a response mediated by Shh that was blocked by 5E1 antibody. The MSC population collected from bone marrow of PBS- or IFNγ-treated mice showed that IFNγ significantly increased the percentage of all MSC cell lines in S phase, with the exception of the stMSCsShhKO cells. While the MSC cell lines with intact Shh expression were recruited to the gastric mucosa in response to IFNγ, stMSCsShhKO were not. Hedgehog signaling is required for MSC proliferation and recruitment to the stomach in response to IFNγ.

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Effect of Th1 cytokines on acid secretion in pharmacologically characterised mouse gastric glands

Cited by 29 publications

References 43 publications

Accelerated Progression of Gastritis to Dysplasia in the Pyloric Antrum of TFF2−/− C57BL6 × Sv129 Helicobacter pylori-Infected Mice

Accelerated Progression of Gastritis to Dysplasia in the Pyloric Antrum of TFF2−/− C57BL6 × Sv129 Helicobacter pylori-Infected Mice

Quercetin and Ellagic Acid in Gastric Ulcer Prevention: An Integrated Scheme of the Potential Mechanisms of Action From in Vivo Study

Sonic Hedgehog Mediates the Proliferation and Recruitment of Transformed Mesenchymal Stem Cells to the Stomach

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