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Published ahead of print on February 11, 2005, doi:10.1164/rccm.200409-1168OC

Am. J. Respir. Crit. Care Med., Volume 171, Number 9, May 2005, 949-957

A more recent version of this article appeared on May 1, 2005
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Submitted on September 10, 2004
Accepted on February 6, 2005

Promoter Analysis and Aberrant Expression of MUC5B gene in Diffuse Panbronchiolitis

Koichiro Kamio1, Ikumi Matsushita2, Minako Hijikata2, Goh Tanaka2, Koh Nakata2, Takafumi Ishida3, Katsushi Tokunaga4, Yoichiro Kobashi5, Yoshio Taguchi6, Sakae Homma7, Koichiro Nakata8, Arata Azuma9, Shoji Kudoh9, and Naoto Keicho2*

1 Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo, Japan; Fourth Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan, 2 Department of Respiratory Diseases, Research Institute, International Medical Center of Japan, Shinjuku-ku, Tokyo, Japan, 3 Unit of Human Biology and Genetics, Department of Biological Sciences, Graduate School of Science, University of Tokyo, Bunkyo-ku, Tokyo, Japan, 4 Department of Human Genetics, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan, 5 Department of Pathology, Tenri Hospital, Tenri, Nara, Japan, 6 Department of Respiratory Medicine, Tenri Hospital, Tenri, Nara, Japan, 7 Department of Respiratory Medicine, Respiratory Center, Toranomon Hospital, Minato-ku, Tokyo, Japan, 8 Department of Pulmonary Medicine, Toho University School of Medicine, Ota-ku, Tokyo, Japan, 9 Fourth Department of Internal Medicine, Nippon Medical School, Bunkyo-ku, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: nkeicho-tky{at}umin.ac.jp.

Diffuse panbronchiolitis (DPB) is a chronic inflammatory airway disease predominantly affecting Asian populations. DPB is considered to be a complex genetic disease. Considering the mucous hypersecretion of the disease, we hypothesized that the transcriptional activity of mucin genes may be altered in DPB. We analyzed nucleotide sequences of regulatory region of six mucin genes MUC1, MUC2, MUC4, MUC5AC, MUC5B and MUC7 and detected their promoter polymorphisms. Among them, insertion/deletion polymorphism identified in the MUC5B gene was significantly associated with the disease (p=0.0001). Transcriptional activity observed in the three major promoter haplotypes corresponded to the strength of the disease association in which these haplotypes are involved. Immunohistochemistry of the lung tissues of DPB revealed that MUC5B was abundantly expressed not only in bronchial glands but also in increased numbers of goblet cells on the bronchial surface, where MUC5AC is predominant and MUC5B expression is generally scarce in the normal lung. Marked mucous hypersecretion observed in DPB may be partly explained by increased and aberrant expression of MUC5B. The possible involvement of MUC5B gene in DPB was demonstrated. A further role of MUC5B polymorphism in its pathogenesis should be studied in the future.
Key words: Disease susceptibility, Polymorphism, Case-control study, Gene expression, Immunohistochemistry




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