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

Elfvin, Anders, 1971 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
Bölin, Ingrid, 1952 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology
Lönroth, Hans, 1952 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
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Fändriks, Lars, 1956 (författare)
Gothenburg University,Göteborgs universitet,Institutionen för kliniska vetenskaper,Institute of Clinical Sciences
visa färre...
 (creator_code:org_t)
2009-07-08
2006
Engelska.
Ingår i: Scandinavian journal of gastroenterology. - : Informa UK Limited. - 0036-5521 .- 1502-7708. ; 41:9, s. 1013-8
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
Stäng  
  • 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.

Nyckelord

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

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