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Laboratory and Animal Investigations |

Inhibition of Monocyte Chemoattractant Protein-1 Expression in Cytokine-Treated Human Lung Epithelial Cells by Thiazolidinedione*

Atsuko Momoi, MD, PhD; Koji Murao, MD, PhD; Hitomi Imachi, MD, PhD; Toshihiko Ishida, MD, PhD; Wen Ming Cao, MD; Makoto Sato, MD, PhD; Jiro Takahara, MD, PhD
Author and Funding Information

*From the First Department of Internal Medicine, Kagawa Medical University, Kita-gun, Kagawa, Japan.

Correspondence to: Koji Murao, MD, First Department of Internal Medicine, Kagawa Medical University, 1750–1, Miki-cho, Kita-gun, Kagawa, 761-0793, Japan; e-mail:mkoji@kms.ac.jp



Chest. 2001;120(4):1293-1300. doi:10.1378/chest.120.4.1293
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Study objective: Several lung diseases are characterized by the presence of increased numbers of activated macrophages. The recruitment and activation of peripheral blood monocytes are potentially critical regulatory events for the control of pulmonary inflammation. The chemokine monocyte chemoattractant protein (MCP)-1 is a potent chemoattractant for monocytes. MCP-1 is produced by lung epithelial cells during the course of inflammatory lung diseases. In the present study, we examined the effects of a thiazolidinedione (TZD), which is used to improve the insulin resistance of individuals with diabetes mellitus, on MCP-1 expression in a human lung epithelial cell line, A549.

Measurements and results: In A549 cells, interleukin (IL)-1β and tumor necrosis factor (TNF)-α induced endogenous MCP-1 protein secretion and messenger RNA expression. The TZD inhibited the increase of MCP-1 secretion by IL-1β and TNF-α treatment. The TZD inhibited the expression of MCP-1 messenger RNA with IL-1β treatment, but not with TNF-α treatment. This observation was confirmed by the results of a monocyte chemotactic assay. The transcriptional activity of human MCP-1 promoter in A549 cells paralleled the endogenous messenger RNA expression by cytokines and TZD treatment.

Conclusions: Our findings indicated that the suppression of the expression of MCP-1 could be accomplished by TZD treatment, raising the possibility that TZD may be of therapeutic value in several lung diseases in which MCP-1 plays an important role.

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