Interleukin 29 activates expression of tissue inhibitor of metalloproteinase 1 in macrophages via toll‑like receptor 2

Zhang,Haoqiang; Song,Bing; He,Shaoheng

doi:10.3892/mmr.2018.8865

Interleukin 29 activates expression of tissue inhibitor of metalloproteinase 1 in macrophages via toll‑like receptor 2

Authors:
- Haoqiang Zhang
- Bing Song
- Shaoheng He
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Affiliations: Department of Endocrinology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China, Department of Ear Nose and Throat, Allergy and Clinical Immunology Research Center, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001, P.R. China
Published online on: April 11, 2018 https://doi.org/10.3892/mmr.2018.8865
Pages: 8363-8368

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Abstract

Obesity and diabetes are characterized by low grade chronic inflammation status and insulin resistance in adipose tissue associated with metalloproteinase inhibitor 1 (TIMP1). Interleukin (IL)29, exhibits multiple immune regulatory activities. However, the role of IL29 and its effects on TIMP1 remain to be elucidated. The present study was designed to investigate the effects of IL29 on expression of TIMP1 in macrophages associated with inflammation in adipose tissue. IL29 and high glucose were used to activate Raw264.7 cells and primary macrophages with or without antibody‑mediated inhibition of toll like receptor (TLR) 2 and TLR4. TIMP1 was measured in culture media of Raw264.7 cells and primary macrophages by ELISA. IL29 and high glucose increased TIMP1 levels in Raw264.7 cells and primary macrophages. Antibody‑mediated inhibition of TLR2 or TLR2 gene knockout decreased TIMP1 levels activated by IL29, however not by high glucose in the medium of Raw264.7 cells and primary macrophages. Furthermore, antibody‑mediated inhibition of TLR4 or TLR4 gene knockout decreased TIMP1 levels which were stimulated by high glucose, not by IL29 in the medium of Raw264.7 cells and primary macrophages. The results of the present study indicate that TLR2 is involved in IL29‑stimulated TIMP1 expression in Raw264.7 cells and primary macrophages.

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