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 journalArticle

4 Citations (Scopus)

Abstract

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
Volume45
DOIs
StatePublished - Jun 1 2014
Externally publishedYes

Fingerprint

Inflammasomes
Embryonic Structures
Interleukin-1
Animals
Enteritis
Enterotoxins
Ablation
Small Interfering RNA
Interleukin-2
Diarrhea
Hot Temperature
Chemical activation
E coli heat-labile enterotoxin
Association reactions
Tissue
Serum

Keywords

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

ASJC Scopus subject areas

  • Toxicology

Cite this

Molecular mechanism for the effects of E. Coli heat-labile enterotoxin on mouse embryo survival. / Li, Wenyan; Han, Dongmei; Liang, Shuang; Zhong, Zhenyu; Li, Xiujin; Wen, Jiexia; Lin, Hongyu; Wang, Liyue; Li, Xiangyun; Zhong, Xiuhui; Zhong, Fei.

In: Reproductive Toxicology, Vol. 45, 01.06.2014, p. 31-38.

Research output: Contribution to journalArticle

Li, Wenyan ; Han, Dongmei ; Liang, Shuang ; Zhong, Zhenyu ; Li, Xiujin ; Wen, Jiexia ; Lin, Hongyu ; Wang, Liyue ; Li, Xiangyun ; Zhong, Xiuhui ; Zhong, Fei. / Molecular mechanism for the effects of E. Coli heat-labile enterotoxin on mouse embryo survival. In: Reproductive Toxicology. 2014 ; Vol. 45. pp. 31-38.
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AU - Wen, Jiexia

AU - Lin, Hongyu

AU - Wang, Liyue

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AB - 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.

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