Molecular mechanism for the effects of E. Coli heat-labile enterotoxin on mouse embryo survival

Wenyan Li, Dongmei Han, Shuang Liang, Zhenyu Zhong, Xiujin Li, Jiexia Wen, Hongyu Lin, Liyue Wang, Xiangyun Li, Xiuhui Zhong, Fei Zhong

Research output: Contribution to journalArticlepeer-review

7 Scopus citations


Heat-labile enterotoxin (LT) can cause animal enteritis and diarrhea. However, the possible association of LT with embryo survival in pregnant animals and the mechanisms involved remain unknown. To investigate the effects of LT on embryo survival, we treated mouse early embryos in vitro and pregnant mice in vivo with recombinant LT. LT significantly decreased mouse embryo survival, and induced IFN-γ, IL-2 and IL-1β production in the serum and placental tissue. LT also triggered IL-1β release from LPS-primed microphages, suggesting LT can activate inflammasomes. To determine the pathway involved in LT-induced inflammasome activation, small interfering RNAs were used to knockdown NLRP3 and ASC, the key components of NLRP3 inflammasome pathway. Ablation of NLRP3 and ASC abolished LT-induced IL-1β release, confirming the involvement of NLRP3 inflammasome. By comparing two subunits of LT, only LTA but not LTB subunit was identified to activate the NLRP3 inflammasome.

Original languageEnglish (US)
Pages (from-to)31-38
Number of pages8
JournalReproductive Toxicology
StatePublished - Jun 2014
Externally publishedYes


  • Cytokines
  • E. coli heat-labile enterotoxin
  • Embryo survival
  • Inflammasome

ASJC Scopus subject areas

  • Toxicology


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