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Infection and Immunity, May 2000, p. 2863-2869, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Role of Activated Protein C in Helicobacter pylori-Associated Gastritis

Satoko Oka,1 Esteban Cesar Gabazza,1,2 Yukiko Taguchi,1 Michihiko Yamaguchi,1 Shigehito Nakashima,1 Koji Suzuki,2 Yukihiko Adachi,1,* and Ichiro Imoto1

The Third Department of Internal Medicine1 and the Department of Molecular Pathobiology,2 Mie University School of Medicine, Tsu, Mie, Japan

Received 7 September 1999/Returned for modification 3 December 1999/Accepted 2 February 2000

The protein C (PC) pathway has recently been suggested to play a role in the regulation of the inflammatory response. To further extend the anti-inflammatory effect of activated PC (APC) in vivo, particularly its biological relevance to human disease, the activity of APC in the mucosa of patients with Helicobacter pylori-associated gastritis and the effect of vacuolating cytotoxin (VacA), cytotoxin-associated antigen (CagA), and H. pylori lipopolysaccharide (LPS) on PC activation were evaluated. This study comprised 35 patients with chronic gastritis. There were 20 patients with and 15 without H. pylori infection. The levels of PC and APC-PC inhibitor (PCI) complex were measured by immunoassays. The level of PC was significantly decreased and the level of APC-PCI complex was significantly increased in biopsy specimens from gastric corpus and antrum in patients with H. pylori-associated gastritis as compared to H. pylori-negative subjects. The concentrations of VacA, CagA, and LPS were significantly correlated with those of the APC-PCI complex in biopsy mucosal specimens from the gastric corpus and antrum. H. pylori LPS, VacA, and CagA induced a dose-dependent activation of PC on the surface of monocytic cells. APC inhibited the secretion of tumor necrosis factor alpha (TNF-alpha ) induced by H. pylori LPS. Overall, these results suggest that H. pylori infection is associated with increased APC generation in the gastric mucosa. The inhibitory activity of APC on TNF-alpha secretion may serve to protect H. pylori-induced gastric mucosal damage.

* Corresponding author. Mailing address: Third Department of Internal Medicine, Mie University School of Medicine, Edobashi 174-2, Tsu, Mie 514-8507, Japan. Phone: 81 59 232 1111. Fax: 81 59 231 5223. E-mail: adachi-y{at}clin.medic.mie-u.ac.jp.

Infection and Immunity, May 2000, p. 2863-2869, Vol. 68, No. 5
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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