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Persistent increase in myofibroblasts in Helicobacter heilmannii-infected mice but not in Helicobacter pylori-infected Mongolian gerbils: colocalization of COX-2 and bFGF immunoreactivity

  1. M. Nakamura1,
  2. S. Takahashi3,
  3. H. Matsui2,
  4. K. Nishikawa3,
  5. Y. Akiba4,
  6. H. Ishii4

Article first published online: 20 APR 2002

DOI: 10.1046/j.1365-2036.16.s2.26.x

Issue

Alimentary Pharmacology & Therapeutics

Alimentary Pharmacology & Therapeutics

Volume 16, Issue Supplement s2, pages 174–179, April 2002

Additional Information

How to Cite

Nakamura, M. , Takahashi, S. , Matsui, H. , Nishikawa, K. , Akiba, Y. and Ishii, H. (2002), Persistent increase in myofibroblasts in Helicobacter heilmannii-infected mice but not in Helicobacter pylori-infected Mongolian gerbils: colocalization of COX-2 and bFGF immunoreactivity. Alimentary Pharmacology & Therapeutics, 16: 174–179. doi: 10.1046/j.1365-2036.16.s2.26.x

Author Information

  1. 1

    Center for Basic Research, the Kitasato Institute, Kitasato University, Japan,

  2. 2

    Kitasato Institute for Life Sciences, Kitasato University, Japan,

  3. 3

    Third Department of Internal Medicine, Kyorin University School of Medicine, Japan,

  4. 4

    Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan

* Dr M. Nakamura, Center for Basic Research, the Kitasato Institute, Kitasato University, 5-9-1 Shirokane, Minato-ku, Tokyo 108-8641, Japan. E-mail: nakamura-m@kitasato.or.jp

Publication History

  1. Issue published online: 20 APR 2002
  2. Article first published online: 20 APR 2002

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Background:

The clinical significance of Helicobacter heilmannii infection remains uncertain, owing to the lack of a specific detection method. Recently, we reported a marked increase in myofibroblasts in the early stage of Helicobacter pylori infection in Monglian gerbils.

Aim:

The present study was designed to clarify changes in myofibroblasts, and in the immunoeactivities of basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase after H. pylori infection in Monglian gerbils and H. heilmannii infection in mice.

Methods:

After oral inoculation, changes in the location of bacteria and the immunoreactivity of myofibroblasts, basic fibroblast growth factor, cyclooxygenase-2 and inducible nitric oxide synthase were stained with the indirect immunofluorescent method and observed by confocal laser microscopy.

Results:

In H. heilmannii-infected mice, the increases in myofibroblasts and in immunoreactivities of these three markers were sustained 12 months after infection. In H. pylori-infected Monglian gerbils, however, these increases were significant at 3 months but had returned to control levels at 12 months.

Conclusions:

Two types of Helicobacter infection showed different patterns of myofibroblast proliferation, coinciding with the extent of inflammation. These findings suggest that this difference may be related to the consequences of the infection.

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