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Am J Physiol Lung Cell Mol Physiol (December 13, 2002). doi:10.1152/ajplung.00211.2002
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Articles in PresS, published online ahead of print December 13, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00211.2002
Submitted on July 3, 2002
Accepted on December 10, 2002

SERINE PROTEASE INHIBITORS MODULATE CHEMOTACTIC CYTOKINE PRODUCTION BY HUMAN LUNG FIBROBLASTS IN VITRO

Hiroki Numanami1, Sekiya Koyama2, Etsuro Sato2, Masayuki Haniuda3, Dan K. Nelson1, Jeffrey C. Hoyt1, Jon L. Freels1, Michael P. Habib1, and Richard A. Robbins1*

1 Research Service, Southern Arizona Veterans Health Care System, Tucson, AZ, USA; Arizona Respiratory Center, Research Service, Southern Arizona Veterans Health Care University of Arizona, Tucson, AZ, USA
2 First Department of Internal Medicine, Shinshu University, Matsumoto, Japan
3 Second Department of Surgery, Shinshu University, Matsumoto, Japan

* To whom correspondence should be addressed. E-mail: Richard.Robbins2{at}med.va.gov.

Chemotactic chemokines can be released from lung fibroblasts in response to interleukin-1{beta} (IL-1{beta}) and tumor necrosis factor-{alpha} (TNF-{alpha}). An imbalance between proteases and antiproteases has been observed at inflammatory sites, and therefore, protease inhibitors might modulate fibroblast release of chemotactic cytokines. To test this hypothesis, serine protease inhibitors (FK706, {alpha}1-antitrypsin, or TLCK) were evaluated for their capacity to attenuate the release of neutrophil chemotactic activity (NCA) or monocyte chemotactic activity (MCA) from human fetal lung fibroblasts (HFL-1). Similarly, the release of the chemoattractants interleukin (IL)-8, granulocyte colony stimulating factor (G-CSF), monocyte chemoattractant protein (MCP)-1, macrophage CSF (M-CSF), and granulocyte-macrophage CSF (GM-CSF), from HLF-1 were evaluated in response to IL-1{beta} and TNF-{alpha}. NCA, MCA and chemotactic cytokines were attenuated by FK706. However, matrix metalloproteinase inhibitors were without effect, and cysteine protease inhibitors only slightly attenuated chemotactic or cytokine release. These data suggest that IL-1{beta} and TNF-{alpha} may stimulate lung fibroblasts to release NCA and MCA by a protease-dependent mechanism and that serine protease inhibitors may attenuate the release.




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