Original Article

Interleukin-13 Induces Tissue Fibrosis by Selectively Stimulating and Activating Transforming Growth Factor ß₁

Correspondence to: Jack A. Elias, Yale University School of Medicine, Section of Pulmonary and Critical Care Medicine, Dept. of Internal Medicine, 333 Cedar St. - 105 LCI, New Haven, CT 06520-8057. Tel:203-785-4163 Fax:203-785-3826 E-mail:jack.elias{at}yale.edu.

Interleukin (IL)-13 is a key mediator of tissue fibrosis caused by T helper cell type 2 inflammation. We hypothesized that the fibrogenic effects of IL-13 are mediated by transforming growth factor (TGF)-ß. To test this hypothesis we compared the regulation of TGF-ß in lungs from wild-type mice and CC10-IL-13 mice in which IL-13 overexpression causes pulmonary fibrosis. IL-13 selectively stimulated TGF-ß₁ production in transgenic animals and macrophages were the major site of TGF-ß₁ production and deposition in these tissues. IL-13 also activated TGF-ß₁ in vivo. This activation was associated with decreased levels of mRNA encoding latent TGF-ß–binding protein-1 and increased mRNA encoding urinary plasminogen activator, matrix metalloproteinase (MMP)-9, and CD44. TGF-ß₁ activation was abrogated by the plasmin/serine protease antagonist aprotinin. It was also decreased in progeny of crosses of CC10-IL-13 mice and MMP-9 null mice but was not altered in crosses with CD44 null animals. IL-13–induced fibrosis was also significantly ameliorated by treatment with the TGF-ß antagonist soluble TGFßR-Fc (sTGFßR-Fc). These studies demonstrate that IL-13 is a potent stimulator and activator of TGF-ß₁ in vivo. They also demonstrate that this activation is mediated by a plasmin/serine protease- and MMP-9–dependent and CD44-independent mechanism(s) and that the fibrogenic effects of IL-13 are mediated, in great extent, by this TGF-ß pathway.

Key Words: lung, plasmin, matrix metalloproteinase-9, CD44, asthma

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