Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 52, Issue -, Pages 24-33Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2017.08.023
Keywords
Epigallocatechin-3-gallate; 67-kDa laminin receptor; Toll-like receptor 4; Acute lung injury; Oxidative stress; H9N2 swine influenza virus
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Funding
- National Natural Science Foundation of China, China [31672522, 31602030]
- Natural Science Foundation of Hebei North University [ZD201306]
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Epigallocatechin-3-gallate (EGCG) was found to inhibit the Toll-like receptor 4 (TLR4) pathway involved in influenza virus pathogenesis. Here, the effect of EGCG on TLR4 in an H9N2 virus-induced acute lung injury mouse model was investigated. BALB/c mice were inoculated intranasally with A/Swine/Hebei/108/2002 (H9N2) virus or noninfectious allantoic fluid, and treated with EGCG and E5564 or normal saline orally for 5 consecutive days. PMVECs were treated with EGCG or anti-67 kDa laminin receptor (LR). Lung physiopathology, inflammation, oxidative stress, viral replication, and TLR4/NF-kappa B/Toll-interacting protein (Tollip) pathway in lung tissue and/or PMVECs were investigated. EGCG attenuated lung histological lesions, decreased lung W/D ratio, cytokines levels, and inhibited MPO activity and prolonged mouse survival. EGCG treatment also markedly downregulated TLR4 and NF-kappa B protein levels but Tollip expression was upregulated compared with that in untreated H9N2-infected mice (P < 0.05). In PMVECs, anti-67LR antibody treatment significantly down regulated Tollip levels; however, the TLR4 and NF-kappa B protein levels dramatically increased compared with that in the EGCG-treated group (P < 0.05). EGCG remarkably downregulated TLR4 protein levels through 67LR/Tollip, decreased MPO activity and inflammatory cytokine levels, supporting EGCG as a potential therapeutic agent for managing acute lung injury induced by H9N2 SIV.
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