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Infection and Immunity, July 2001, p. 4382-4389, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4382-4389.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Type I Helicobacter pylori Lipopolysaccharide Stimulates Toll-Like Receptor 4 and Activates Mitogen Oxidase 1 in Gastric Pit Cells

Tsukasa Kawahara,1 Shigetada Teshima,1 Ayuko Oka,1 Toshiro Sugiyama,2 Kyoichi Kishi,1 and Kazuhito Rokutan1,*

Department of Nutritional Physiology, School of Medicine, University of Tokushima, Tokushima 770-8503,1 and the Third Department of Internal Medicine, Hokkaido University School of Medicine, Sapporo 060-8638,2 Japan

Received 16 April 2001/Accepted 21 April 2001

Guinea pig gastric pit cells express an isozyme of gp91-phox, mitogen oxidase 1 (Mox1), and essential components for the phagocyte NADPH oxidase (p67-, p47-, p40-, and p22-phox). Helicobacter pylori lipopolysaccharide (LPS) and Escherichia coli LPS have been shown to function as potent activators for the Mox1 oxidase. These cells spontaneously secreted about 10 nmol of superoxide anion (O2-)/mg of protein/h under LPS-free conditions. They expressed the mRNA and protein of Toll-like receptor 4 (TLR4) but not those of TLR2. LPS from type I H. pylori at 2.1 endotoxin units/ml or higher stimulated TLR4-mediated phosphorylations of transforming growth factor beta -activated kinase 1 and its binding protein 1 induced TLR4 and p67-phox and up-regulated O2- production 10-fold. In contrast, none of these events occurred with H. pylori LPS from complete or partial deletion mutants of the cag pathogenicity island. Lipid A was confirmed to be a bioactive component for the priming effects, while removal of bisphosphates from lipid A completely eliminated the effects, suggesting the importance of the phosphorylation pattern besides the acylation pattern for the bioactivity. H. pylori LPS is generally accepted as having low toxicity; however, our results suggest that type I H. pylori lipid A may be a potent stimulator for innate immune responses of gastric mucosa by stimulating the TLR4 cascade and Mox1 oxidase in pit cells.

* Corresponding author. Mailing address: Department of Nutrition, School of Medicine, University of Tokushima, 3-18-15 Kuramoto-cho, Tokushima 770-8503, Japan. Phone: 81-88-633-9246. Fax: 81-88-633-7086. E-mail: rokutan{at}nutr.med.tokushima-u.ac.jp.

Infection and Immunity, July 2001, p. 4382-4389, Vol. 69, No. 7
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.7.4382-4389.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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