Increased expression of inducible nitric oxide synthase and peroxynitrite in Helicobacter Pylori gastric ulcer

Sakaguchi, Aya; Miura, Soichiro; Takeuchi, T; Hokari, Ryota; Mizumori, Misa; Yoshida, Hideo; Higuchi, Hajime; Mori, Mikiji; Kimura, Hiroyuki; Suzuki, Hidekazu; Ishii, Hiromasa

doi:10.1016/s0891-5849(99)00124-0

Cited by 43 publications

(33 citation statements)

References 31 publications

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“…Guo et al (11) reported induction of iNOS expression by IFN-␥ in vitro using human epithelial cells. iNOS mRNA induction by H. pylori in vitro and in H. pylori-positive gastritis biopsies has been reported (9,10,24). In addition, since COX-2 mRNA expression was unchanged in all treatment groups, it appears that iNOS and COX-2 are not coregulated at the transcriptional level in gastric tissue.…”

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confidence: 72%

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Role of Gamma Interferon inHelicobacter pyloriInduction of Inflammatory Mediators during Murine Infection

Obonyo¹,

Guiney²,

Harwood³

et al. 2002

Infect Immun

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confidence: 72%

“…In addition to these effectors, inducible forms of cyclooxygenase 2 (COX-2) and nitric oxide synthase (iNOS) have been shown to be upregulated during H. pylori gastritis (9,10,18,24). Induction of COX-2 may contribute to either mucosal protection or inflammation during bacterial infection (9,32).…”

mentioning

confidence: 99%

Role of Gamma Interferon inHelicobacter pyloriInduction of Inflammatory Mediators during Murine Infection

Obonyo¹,

Guiney²,

Harwood³

et al. 2002

Infect Immun

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“…In addition to determining the predominance of Th1 cytokines, previous studies determined that Helicobacter infection leads to upregulation of iNOS, which has been implicated in DNA damage, apoptosis, carcinogenesis, and the cytotoxicity observed in Helicobacter infections (15,21,28,31). Previous studies have shown that patients infected with H. pylori have higher levels of both oxidized and nitrated proteins and increased iNOS expression than uninfected humans do (24,40).…”

Section: Discussionmentioning

confidence: 99%

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

et al. 2005

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Persistent Helicobacter felis infection in (C57BL/6 ؋ 129SvEv)F 1 mice induces chronic gastritis. Expression of inducible nitric oxide synthase (iNOS) is upregulated in response to Helicobacter infection. In this study, 20 10-week-old iNOS ؊/؊ mice and 20 wild-type [(C57BL/6 ؋ 129SvEv)F 1 ] mice were infected with H. felis by oral gavage and were assessed histologically and serologically at 32 weeks postinfection. Equal numbers of uninfected controls were sham inoculated. The mice were scored for severity of gastric inflammation, hyperplasia, glandular atrophy, and mucous metaplasia in the corpus and for the level of helicobacter colonization. The immunoglobulin G1 (IgG1), IgG2a, and IgG2c antibody responses to H. felis were determined. As a secondary measure, serum cholesterol levels were assessed. iNOS ؊/؊ mice have a propensity for increased serum cholesterol, and although controversial, several human epidemiologic studies have demonstrated an association between Helicobacter infection and several risk factors for cardiovascular disease, including elevated serum cholesterol. Nevertheless, no differences in serum cholesterol levels were observed between the H. felis-infected and -uninfected iNOS ؊/؊ mice in this study. The uninfected animals had minimal to no gastric pathology. The gastric pathology scores for the infected animals were reduced significantly in the iNOS-deficient mice relative to those for the wild-type mice (all P < 0.01). Helicobacter-infected iNOS ؊/؊ mice had chronic lymphoid infiltration and negligible to mild glandular atrophy and mucous metaplasia in the fundic mucosa, while H. felis-infected wild-type mice had severe atrophic and metaplastic mucosal changes. The atrophic gastritis in the infected wild-type mice, particularly the female mice, was also accompanied by greater granulocytic infiltration, antral hyperplasia, and diminished antral colonization, unlike that in the infected iNOS ؊/؊ mice. iNOS

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“…pylori produces ammonia from urea in the host stomach with urease, neutralizes the gastric acid, and multiplies in the neutralized mucin layer of the host stomach [43]. Activation of the phagocyte oxidative metabolism by H. pylori [48], alterations in gastric juice ascorbic acid concentrations in H. pylori-seropositive patients [49], and increased expression of inducible nitric oxide synthase and peroxynitrite induced by H. pylori [50] have been demonstrated.…”

Section: H Pylori Infection and Host Responsesmentioning

confidence: 99%

Helicobacter pylori infection and gastric carcinogenesis in animal models

2003

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Increased expression of inducible nitric oxide synthase and peroxynitrite in Helicobacter Pylori gastric ulcer

Cited by 43 publications

References 31 publications

Role of Gamma Interferon inHelicobacter pyloriInduction of Inflammatory Mediators during Murine Infection

Role of Gamma Interferon inHelicobacter pyloriInduction of Inflammatory Mediators during Murine Infection

GastricHelicobacterInfection Induces a Th2 Phenotype but Does Not Elevate Serum Cholesterol in Mice Lacking Inducible Nitric Oxide Synthase

Helicobacter pylori infection and gastric carcinogenesis in animal models

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