Gastric mucosal hyperplasia via upregulation of gastrin induced by persistent activation of gastric innate immunity in major histocompatibility complex class II deficient mice

Fukui, Toshiro; Nishio, Akiyoshi; Okazaki, Kazuichi; Uza, Norimitsu; Ueno, S.; Kido, Masahiro; Inoue, Satoko; Kitamura, Hiroshi; Kiriya, Keiichi; Asada, Masanori; Tamaki, Hiroyuki; Matsuura, Minoru; Kawasaki, Kohkichi; Suzuki, Kazuyuki; Uchida, Kazushige; Fukui, Hirokazu; Nakase, Hiroshi; Watanabe, Norihiko; Chiba, Tsutomu

doi:10.1136/gut.2005.077917

Cited by 14 publications

(12 citation statements)

References 35 publications

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“…Also, recent studies from the same group have revealed that GR and histamine receptor antagonists inhibit gastric carcinogenesis [28]. In addition, Fukui et al [29 ]have reported that the gastrin-GR system contributes to mucosal hypertrophic changes in major-histocompatibility-complex-class-II-deficient mice and examined the involvement of the innate local immune status in the gastric mucosa. However, another report has demonstrated that independently of gastrin, achlorhydria is the main cause of premalignant changes and that gastrin is essential for the prevention of gastric disease [30].…”

Section: Discussionmentioning

confidence: 99%

Role of the Gastrin-Gastrin Receptor System in the Expansive Growth of Human Gastric Neoplasms

et al. 2008

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Background and Aim: Gastrin is one of the most important gut hormones. However, the role of the gastrin-gastrin receptor (GR) system in the growth of gastric tumors is still unclear. Methods: We examined serum gastrin levels in 957 patients with early gastric carcinoma. Next, we raised antibody against the GR and examined GR expression in 5 gastric carcinoma cell lines and 48 human gastric tumor tissues. In 28 cases, Helicobacter pylori eradication therapy was performed and morphological tumor changes were examined. Results: Serum gastrin levels were significantly higher in patients with elevated tumors than in patients with depressed tumors (p = 0.02). All gastric carcinoma cell lines expressed GR. Thirty-one of 48 (65%) gastric tumors expressed GR, and its expression was prominent in elevated-type tumor with an intestinal histologic feature. Of 28 patients who underwent eradication therapy, 9 showed gastric tumors that became flat or depressed. In these 9 cases, GR expression was detected in all tumors, and the decrease in gastrin levels was more prominent than in those without morphological change (p = 0.01). Conclusion: The gastrin-GR system plays an important role in the elevated morphology of gastric tumors.

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Section: Discussionmentioning

confidence: 99%

Role of the Gastrin-Gastrin Receptor System in the Expansive Growth of Human Gastric Neoplasms

et al. 2008

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“…Gastric and intestinal epithelial cells constitutively express TLR2, TLR4 and MD-2 [80,81] and the intestinal myofibroblasts express increased levels of TLR2, TLR3, TLR4, TLR6 and TLR7 after LPS or LTA stimulation [82]. TLR5 is only expressed in intestinal epithelial cells (IEC) in the basolateral membrane under normal circumstances, which may be important for the maintenance of GI homeostasis since flagellin from commensal bacteria generally does not translocate to the basolateral membrane thereby does not induce inflammatory responses [83].…”

Section: Gastrointestinal (Gi) Diseasesmentioning

confidence: 98%

Toll-like receptors in inflammation, infection and cancer

Chen

Huang

Gong

et al. 2007

International Immunopharmacology

299

261

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“…Gastric mucosal hyperplasia is characterized by increased macrophage infiltration and an up-regulated expression of pro-inflammatory IL-1β, TNF-α and COX-2 (Fukui et al, 2006). Granulocyte and macrophage infiltration is increased at the ulcer margin, and it has been suggested that this could be the major source of increased COX-2 expression that is positively regulated by IL-1β and TNF-α Shigeta et al, 1998;Jackson et al, 2000).…”

Section: Figurementioning

confidence: 99%

Carbon monoxide released from its pharmacological donor, tricarbonyldichlororuthenium (II) dimer, accelerates the healing of pre‐existing gastric ulcers

Magierowski

Magierowska

Hubalewska-Mazgaj

et al. 2017

British J Pharmacology

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BACKGROUND AND PURPOSECarbon monoxide (CO), a gaseous mediator produced by haem oxygenases (HOs), has been shown to prevent stress-, ethanol-, aspirin-and alendronate-induced gastric damage; however, its role in gastric ulcer healing has not been fully elucidated. We investigated whether CO released from tricarbonyldichlororuthenium (II) dimer (CORM-2) can affect gastric ulcer healing and determined the mechanisms involved in this healing action. EXPERIMENTAL APPROACHGastric ulcers were induced in Wistar rats by serosal application of acetic acid. Animals received 9 days of treatment with RuCl 3 [2.5 mg·kg À1 intragastrically (i.g.)], haemin (5 mg·kg À1 i.g.), CORM-2 (0.1-10 mg·kg À1 i.g.) administered alone or with zinc protoporphyrin IX (ZnPP, 10 mg·kgGastric ulcer area and gastric blood flow (GBF) were assessed planimetrically, microscopically and by laser flowmeter respectively. Gastric mRNA/protein expressions of EGF, EGF receptors, VEGFA, HOs, nuclear factor (erythroid-derived 2)-like 2 (Nrf2), COX-2, hypoxia-inducible factor (HIF)-1α and pro-inflammatory iNOS, IL-1β and TNF-α were determined by real-time PCR or Western blots. KEY RESULTSCORM-2 and haemin but not RuCl 3 or ZnPP decreased ulcer size while increasing GBF. These effects were reduced by ODQ, indomethacin, L-NNA and glibenclamide. CORM-2 significantly decreased the expression of pro-inflammatory markers, Nrf2/HO1 and HIF-1α, and up-regulated EGF. CONCLUSIONS AND IMPLICATIONSCO released from CORM-2 or endogenously produced by the HO1/Nrf2 pathway accelerates gastric ulcer healing via an increase in GBF, an up-regulation in EGF expression and down-regulation of the inflammatory response.

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Gastric mucosal hyperplasia via upregulation of gastrin induced by persistent activation of gastric innate immunity in major histocompatibility complex class II deficient mice

Cited by 14 publications

References 35 publications

Role of the Gastrin-Gastrin Receptor System in the Expansive Growth of Human Gastric Neoplasms

Role of the Gastrin-Gastrin Receptor System in the Expansive Growth of Human Gastric Neoplasms

Toll-like receptors in inflammation, infection and cancer

Carbon monoxide released from its pharmacological donor, tricarbonyldichlororuthenium (II) dimer, accelerates the healing of pre‐existing gastric ulcers

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