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7. Irradiation Stimulates Human Lung Fibroblasts to Release Inflammatory Cell Chemotactic Activity

Author

KURAI, Makoto and KOYAMA, Sekiya

Subjects
irradiation, IL-8, human lung fibroblast, respiratory system, chemotaxis, MCP-1
Abstract

Background :Radiation therapy plays an important role in the treatment of lung cancer. However, it also radiation therapy often induces serious complications such as radiation-induced pneumonitis and its underlying mechanism remains to be elucidated. Objectives :The present study examined whether radiation might stimulate human lung fibroblasts (HLF)to release neutrophil and monocyte chemotactic activity (NCA and MCA). Methods :HLF were exposed to varying doses of radiation (3-12 Gy)at varying incubation times (12-72 hr). The chemotaxis assays of NCA and MCA were performed by a 48-well microchemotaxis chamber method. The effect of polyclonal antibodies of various cytokines on NCA and MCA was evaluated.Furthermore, the protein and mRNA expression of these effective cytokines was assessed by ELISA and RT-PCR. Results :HLF released NCA and MCA in response to irradiation in a dose-and time-dependent manner. NCA was significantly inhibited by anti-interleukin (IL)-8 antibody and MCA was significantly attenuated by antimonocyte chemoattractant protein (MCP)-1 antibody. The protein secretion of IL-8 and MCP-1 was significantly increased by irradiation, and mRNA expression of IL-8 and MCP-1 was upregulated by irradiation. Conclusion :These findings suggest that HLF may,at least partly,participate in the development of radiationinduced pneumonitis., Article, 信州医学雑誌. 58(2): 57-68 (2010)

Published
2010

30. Serine protease inhibitors modulate chemotactic cytokine production by human lung fibroblasts in vitro.

Author

Numanami H, Koyama S, Sato E, Haniuda M, Nelson DK, Hoyt JC, Freels JL, Habib MP, and Robbins RA

Subjects
Antineoplastic Agents pharmacology, Cells, Cultured, Chemokine CCL2 genetics, Fibroblasts cytology, Fibroblasts drug effects, Gene Expression drug effects, Gene Expression immunology, Granulocyte-Macrophage Colony-Stimulating Factor metabolism, Humans, In Vitro Techniques, Interleukin-1 pharmacology, Interleukin-8 biosynthesis, Interleukin-8 genetics, Pancreatic Elastase pharmacology, RNA, Messenger analysis, Tosyllysine Chloromethyl Ketone pharmacology, Tumor Necrosis Factor-alpha pharmacology, alpha 1-Antitrypsin pharmacology, Benzoates pharmacology, Chemokine CCL2 metabolism, Fibroblasts metabolism, Interleukin-8 metabolism, Lung cytology, Pyrrolidines pharmacology, Serine Proteinase Inhibitors pharmacology
Abstract

Chemotactic chemokines can be released from lung fibroblasts in response to interleukin (IL)-1beta and tumor necrosis factor (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 (FK-706, alpha(1)-antitrypsin, or N(alpha)-p-tosyl-L-lysine chloromethyl ketone) 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 IL-8, granulocyte colony-stimulating factor, monocyte chemoattractant protein-1, macrophage colony-stimulating factor, and granulocyte/macrophage colony-stimulating factor, from HFL-1, were evaluated in response to IL-1beta and TNF-alpha. NCA, MCA, and chemotactic cytokines were attenuated by FK-706. However, matrix metalloproteinase inhibitors were without effect, and cysteine protease inhibitors only slightly attenuated chemotactic or cytokine release. These data suggest that IL-1beta 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.

Published
2003
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