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(Journal of Leukocyte Biology. 2003;73:525-529.)
© 2003 by Society for Leukocyte Biology

NF-B-dependent lymphocyte hyperadhesiveness to synovial fibroblasts by hypoxia and reoxygenation: potential role in rheumatoid arthritis

Myung-Kwan Han^*, Jong-Suk Kim, Byung-Hyun Park, Jung-Ryul Kim^,, Byung-Yun Hwang^,, Hak-Yong Lee^¶,, Eun-Kyung Song^* and Wan-Hee Yoo^,¶

Departments of
^* Microbiology,
Biochemistry,
Orthopedic Sugery, and
^¶ Internal Medicine, and
Research Institute of Clinical Medicine, Chonbuk National University Medical School, Chonju, Korea

Correspondence: Wan-Hee Yoo, M.D., Ph.D., Division of Rheumatology, Department of Internal Medicine, Chonbuk National University Medical School and Research Institute of Clinical Medicine, #634-18, Keum-Am Dong, Duck-Jin Gu, Chonju, Chonbuk, 561-712, Korea. E-mail: ywhim{at}moak.chonbuk.ac.kr

Hypoxia/reoxygenation has been incriminated as a major factor in the pathogenesis of ischemia/reperfusion injury in various ischemic diseases such as rheumatoid arthritis (RA). In this study, we have investigated the effect of hypoxia/reoxygenation on the expression of intercellular adhesion molecule-1 (ICAM-1) in synovial fibroblasts and adherence of lymphocytes to synovial fibroblasts. Hypoxia/reoxygenation strongly activated nuclear factor-B (NF-B) in synovial fibroblasts to the levels produced by phorbol 12-myristate 13-acetate and caused lymphocyte hyperadhesiveness to synovial fibroblasts as well as up-regulation of ICAM-1, both of which were completely blocked by a NF-B antagonist (pyrrolidine dithiocarbamate). These results indicate that hypoxia/reoxygenation has a major role in sequestration of inflammatory cells to synovium mediated by the activation of NF-B. Our data suggest that hypoxia/reoxygenation could be an important target for the development of new, therapeutic strategies in RA.

Key Words: adhesion • synovial fibroblasts

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