English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Activation of Toll-like receptor 4 (TLR4) and its accessory proteins myeloid differentiation protein 2 (MD-2) can trigger immune and inflammatory activities, and contribute to developing chronic inflammatory diseases. The formation of the TLR4/MD-2 complex after binding to lipopolysaccharide (LPS) leads to the activation of downstream signaling pathway. The present study was designed to reveal the effect of the soluble form of the extracellular TLR4 domain and MD-2 (sTLR4/sMD-2) complex lacking the intracellular and transmembrane domains on various aspects of LPS-induced inflammation in vivo and in vitro . It was demonstrated that the sTLR4/sMD-2 complex inhibited the LPS-induced production of tumor necrosis factor-α, interleukin-8 and C-X-C motif chemokine ligand 1 (CXCL1) in THP-1 cells. In addition, it was revealed that the sTLR4/sMD-2 complex significantly reduced LPS-induced acute lung injury (ALI) with a reduction of total cells and neutrophil count, pro-inflammatory cytokines and chemokine CXCL1 in bronchoalveolar lavage fluid. Moreover, the sTLR4/sMD-2 complex inhibited the number of inflammatory cells in the lung of treated animals. These novel mechanisms emphasized the important role of sTLR4/sMD-2 complex in ALI and suggested sTLR4/sMD-2 complex could provide an anti-inflammatory strategy for treating inflammatory diseases.

sTLR4/sMD‑2 complex alleviates LPS‑induced acute lung injury by inhibiting pro‑inflammatory cytokines and chemokine CXCL1 expression