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

doi:10.1016/j.reprotox.2014.01.005

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 journal › Article › peer-review

5 Scopus citations

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 language	English (US)
Pages (from-to)	31-38
Number of pages	8
Journal	Reproductive Toxicology
Volume	45
DOIs	https://doi.org/10.1016/j.reprotox.2014.01.005
State	Published - Jun 2014
Externally published	Yes

Keywords

Cytokines
E. coli heat-labile enterotoxin
Embryo survival
Inflammasome

ASJC Scopus subject areas

Toxicology

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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, 06.2014, p. 31-38.

Research output: Contribution to journal › Article › peer-review

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

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.",

keywords = "Cytokines, E. coli heat-labile enterotoxin, Embryo survival, Inflammasome",

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

note = "Funding Information: This work was supported by the National Natural Science Foundation of China ( 31140093 ) and State Key Research Program ( 2011BAD34B02 ) and the Natural Science Foundation of Hebei Province ( C2013204130 ).",

year = "2014",

month = jun,

doi = "10.1016/j.reprotox.2014.01.005",

language = "English (US)",

volume = "45",

pages = "31--38",

journal = "Reproductigve Toxicoloy",

issn = "0890-6238",

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T1 - Molecular mechanism for the effects of E. Coli heat-labile enterotoxin on mouse embryo survival

AU - Li, Wenyan

AU - Han, Dongmei

AU - Liang, Shuang

AU - Zhong, Zhenyu

AU - Li, Xiujin

AU - Wen, Jiexia

AU - Lin, Hongyu

AU - Wang, Liyue

AU - Li, Xiangyun

AU - Zhong, Xiuhui

AU - Zhong, Fei

N1 - Funding Information: This work was supported by the National Natural Science Foundation of China ( 31140093 ) and State Key Research Program ( 2011BAD34B02 ) and the Natural Science Foundation of Hebei Province ( C2013204130 ).

PY - 2014/6

Y1 - 2014/6

N2 - 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.

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.

KW - Cytokines

KW - E. coli heat-labile enterotoxin

KW - Embryo survival

KW - Inflammasome

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

Abstract

Keywords

ASJC Scopus subject areas

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