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Crosstalk between Toll-like receptor 3 and Notch signaling contributes to CD14+ monocytes activity in enterovirus 71 infected hand, foot, and mouth disease.

Abstract：

:Interaction between Toll-like receptor (TLR) and Notch signaling contributes to inflammatory response in nephropathy and fungicidal infection, however, the role of this crosstalk remains not fully elucidated in enterovirus 71 (EV71)-induced hand, foot, and mouth disease (HFMD). The aim of this study was to investigate the crosstalk between TLR and Notch in inflammatory regulation in EV71 infection. Thirty-seven EV-71-indcued HFMD (16 mild and 21 severe cases) and eleven normal control (NC) were enrolled. CD14+ monocytes were purified, and were stimulated with either TLR3/4 agonists [poly(I: C) or LPS] or Notch signaling inhibitor. TLRs and Notch receptors expression, proinflammatory cytokines production, and important molecules in signaling pathways were measured by real-time PCR, ELISA, and Western blot. TLR3 and TLR4 was significantly elevated in CD14+ monocytes from HFMD patients than NC. Notch1 and Notch2 mRNA was also remarkably increased in CD14+ monocytes from severe HFMD. Poly(I: C) stimulation resulted in robust increase of IL-8, IL-6, and TNF-α by CD14+ monocytes in severe HFMD compared to NC. Activation of Notch1, Notch2, and target genes, Hes1 and Hes5 was also enhanced upon ploy(I: C) treatment. Although inhibition of Notch signaling did not affect TLR3 expression, poly(I: C)-induced inflammatory response was robustly attenuated, which was accompanied by silencing Src phosphorylation in CD14+ monocytes from severe HFMD patients. The current data indicated that crosstalk between TLR3 and Notch signaling modulated CD14+ monocytes function and inflammatory responses in the progression of EV71-induced HFMD.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Hao J,Li P,Tian Y,Wang Y,Li S,Wang L,Li S

doi

10.1016/j.intimp.2018.04.031

subject

Has Abstract

pub_date

2018-07-01 00:00:00

pages

26-33

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(18)30182-6

journal_volume

60

pub_type

杂志文章

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