Are individuals with lower neutrophil oxidative burst activity more prone to Helicobacter pylori infection?

Helicobacter pylori infection has been reported to cause enhanced reactive oxygen species in the gastric mucosa. We examined the relationship between H. pylori infection and neutrophil function of peripheral blood. The subjects were 904 volunteers who participated in the Iwaki Health Promotion Proje...

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Veröffentlicht in:Luminescence 2008-05, Vol.23 (3), p.132-138
Hauptverfasser: Matsuzaka, Masashi, Fukuda, Shinsaku, Yamai, Kiyonori, Tsuya, Ryousuke, Fukuoka, Yu, Takahashi, Ippei, Yaegaki, Makoto, Shimoyama, Tadashi, Sakamoto, Juichi, Umeda, Takashi, Nakaji, Shigeyuki
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Sprache:eng
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Zusammenfassung:Helicobacter pylori infection has been reported to cause enhanced reactive oxygen species in the gastric mucosa. We examined the relationship between H. pylori infection and neutrophil function of peripheral blood. The subjects were 904 volunteers who participated in the Iwaki Health Promotion Project in 2005. 158 subjects who were infected with H. pylori in 2005 also participated in this project in 2006 and were categorized into two groups: the eradication group, in which H. pylori was successfully eradicated during the 12 month period, and the non‐eradication group, in which eradication was unsuccessful or the subjects did not receive eradication therapy. The laboratory assays performed were: a titre of H. pylori antibody; neutrophil counts; and oxidative burst activity (OBA) of neutrophils. Logistic regression analysis was executed, with H. pylori infection as the dependent variable and other items as the independent variables. OBA showed an inverse association with H. pylori infection in 2005. Additionally, when comparing the eradication and non‐eradication groups, the change rates of OBA between 2005 and 2006 did not show any significant difference. It was concluded that H. pylori infection does not lower OBA, but those individuals in whom OBA was lower were more prone to H. pylori infection. Copyright © 2008 John Wiley & Sons, Ltd.
ISSN:1522-7235
1522-7243
1099-1271
DOI:10.1002/bio.1022