Open AccessNLRP3 inflammasome is responsible for Hantavirus inducing interleukin-1β in THP-1 cells
Author(s) -
Wei Ye,
Yingfeng Lei,
Mengmeng Yu,
Yongni Xu,
Mengyuan Cao,
Yu Lan,
Liang Zhang,
Puyuan Li,
Wentao Bai,
Xu Zhang,
Fanglin Zhang
Publication year - 2015
Publication title -
international journal of molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.048
H-Index - 90
eISSN - 1791-244X
pISSN - 1107-3756
DOI - 10.3892/ijmm.2015.2162
Subject(s) - inflammasome , thp1 cell line , oncogene , molecular medicine , interleukin , hantavirus , biology , virology , cell cycle , apoptosis , cancer research , medicine , immunology , inflammation , cell culture , cytokine , virus , genetics
Persistent high fever is one typical clinical symptom of hemorrhagic fever with renal syndrome (HFRS) and circulating interleukin-1β (IL-1β) is elevated throughout HFRS. The mechanisms responsible for viral induction of IL-1β secretion are unknown. In the present study, Hantaan virus (HTNV) induced the secretion of IL-1β in the human monocytic cell line THP-1. Induction of IL-1β by HTNV relies on the activation of caspase-1. Small hairpin RNA knockdown in HTNV-infected THP-1 cells indicated that nucleotide-binding domain, leucine-rich repeat containing protein 3 (NLRP3) recruits the adaptor apoptosis-associated speck-like protein and caspase-1 to form an NLRP3 inflammasome complex, crucial for the induction of IL-1β. In HTNV-infected THP-1 cells, reactive oxygen species release, but not extracellular adenosine triphosphate, was crucial for IL-1β production. In conclusion, Hantavirus induces the formation of the NLRP3 inflammasome in THP-1 cells and this may be responsible for the elevated IL-1β levels in HFRS patients.