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Gastric expression of inducible nitric oxide synthase and myeloperoxidase in relation to nitrotyrosine in Helicobacter pylori-infected Mongolian gerbils.

Artikel i vetenskaplig tidskrift
Författare Anders Elfvin
Ingrid Bölin
Hans Lönroth
Lars Fändriks
Publicerad i Scandinavian journal of gastroenterology
Volym 41
Nummer/häfte 9
Sidor 1013-8
ISSN 0036-5521
Publiceringsår 2006
Publicerad vid Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi
Institutionen för kliniska vetenskaper
Sidor 1013-8
Språk en
Länkar dx.doi.org/10.1080/0036552060063353...
Ämnesord Animals, Blotting, Western, Disease Models, Animal, Gastric Mucosa, metabolism, microbiology, Gerbillinae, Helicobacter Infections, metabolism, microbiology, Helicobacter pylori, pathogenicity, Male, Nitric Oxide Synthase Type II, biosynthesis, Peroxidase, biosynthesis, Pyloric Antrum, metabolism, Pylorus, metabolism, Rats, Severity of Illness Index, Tyrosine, analogs & derivatives, biosynthesis
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

OBJECTIVE: For obscure reasons Helicobacter pylori infection of the gastric mucosa is maintained despite a pronounced host defence response. The present study elucidates possible H. pylori-related interference in the oxy- and nitro-radical formation pathways. MATERIAL AND METHODS: Male Mongolian gerbils were infected with two different H. pylori strains, TN2GF4 and SS1. At 3, 6, 12 or 18 months after inoculation, gastric expressions of myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS) and nitrotyrosine were assessed by Western blotting. RESULTS: Expression of both iNOS and MPO was markedly up-regulated in the H. pylori-infected animals compared with non-infected controls. The TN2GF4-infected animals initially (at 3 and 6 months) demonstrated pronounced expression of both iNOS and MPO. The SSI-infected animals exhibited a slower onset with significantly increased iNOS after 12 and 18 months. Nitrotyrosine expression was slightly elevated in the infected groups at 3 and 6 months compared with that in the controls. Nitrotyrosine levels then decreased and were no longer significantly different from those of controls (TN2GF4-infected animals) or were lower (SS1-infected animals) than in the controls. CONCLUSIONS: The results indicate that peroxynitrite formation as reflected by nitrotyrosine expression is low or even inhibited in chronic H. pylori infection despite pronounced expression of enzymes representing both the oxy- and nitro-radical formation pathways. The results support the theory that H. pylori survival is related to functional inhibition of mucosal enzymatic NO and/or oxy-radical formation.

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