LPS enhances TLR4 expression and IFN‑γ production via the TLR4/IRAK/NF‑κB signaling pathway in rat pulmonary arterial smooth muscle cells

Wang,Pengyan; Han,Xuhui; Mo,Biwen; Huang,Guojin; Wang,Changming

doi:10.3892/mmr.2017.6983

LPS enhances TLR4 expression and IFN‑γ production via the TLR4/IRAK/NF‑κB signaling pathway in rat pulmonary arterial smooth muscle cells

Authors:
- Pengyan Wang
- Xuhui Han
- Biwen Mo
- Guojin Huang
- Changming Wang
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Affiliations: Division of Respiratory Diseases, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China
Published online on: July 14, 2017 https://doi.org/10.3892/mmr.2017.6983
Pages: 3111-3116
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The aim of the present study was to investigate the role of the Toll‑like receptor (TLR)4 signaling pathway in cellular response to lipopolysaccharide (LPS) in rat pulmonary artery smooth muscle cells (PASMCs). Chronic obstructive pulmonary disease (COPD) rats were established with passive inhaling cigarette smoke plus injection of LPS. The TLR4 protein in lung tissues was determined with immunohistochemical staining and protein levels of the components of the TLR4 pathway in PASMCs were analyzed with western blotting. The production of interferon (IFN)‑γ upon LPS stimulation in PASMCs was measured with ELISA. TLR4 expression in lung tissue from COPD rats was increased obviously compared with that in normal group. LPS enhances TLR4 expression in rat PASMCs and induced production of IFN‑γ dramatically. LPS treatment resulted in increased phosphor‑interleukin‑1 receptor‑associated kinase (IRAK), IκB and IκB kinase, as well as the total protein of nuclear factor (NF)‑κB p65. TLR4 inhibitor TAK‑242, IRAK1/4 inhibitor and NF‑κB inhibitor Bay 117082 were capable of suppressing the effects of LPS. TLR4 signaling pathway is functional in PASMCs, and may be involved in the inflammatory response during the pathogenesis of COPD.

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