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Respiratory syncytial virus infection inhibits TLR4 signaling via up‐regulation of miR‐26b
Author(s) -
Liu Shuang,
Gao Li,
Wang Xia,
Xing Yan
Publication year - 2015
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10518
Subject(s) - tlr4 , peripheral blood mononuclear cell , bronchiolitis , biology , virus , messenger rna , in vitro , immune system , respiratory system , immunology , virology , gene , biochemistry , anatomy
Respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract illnesses in infants worldwide. TLR4 signal pathway plays a critical role in regulating immune response against RSV infection. However, the activation of TLR4 in RSV infection is still unclear. In present study, the expression levels of miR‐26b and TLR4 mRNA were detected in peripheral blood mononuclear cells (PBMCs) of children with or without RSV infected bronchiolitis. The expression levels of TLR4 and its downstream genes IFNβ and CCL5 were also quantified in PBMCs infected with RSVΔG or RSV A2 in vitro. The results showed that children with RSV infection had higher miR‐26b level and lower TLR4 mRNA level in PBMCs. miR‐26b was predicted to target TLR4. In vitro, miR‐26b mimic markedly down‐regulated TLR4 mRNA/protein expression and IFNβ/CCL5 concentrations while miR‐26b inhibitor up‐regulated these levels. This study reveals that RSV infection inhibits TLR4 signaling via up‐regulation of miR‐26b, which provides a potential therapeutic target for preventing and treating RSV infection.