Effect of oral exposure to trichloroethylene on JMJD3 expression and polarization of M1 Kupffer cells

HUANG Hua; DING Baiwang; ZUO Xulei; YANG Yi; PENG Jiale; WANG Yican; ZHANG Jiaxiang; ZHU Qixing

doi:10.11836/JEOM21242

Volume 39 Issue 1

Jan. 2022

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Journal of Environmental and Occupational Medicine > 2022 > 39(1): 65-70. > DOI: 10.11836/JEOM21242

HUANG Hua, DING Baiwang, ZUO Xulei, YANG Yi, PENG Jiale, WANG Yican, ZHANG Jiaxiang, ZHU Qixing. Effect of oral exposure to trichloroethylene on JMJD3 expression and polarization of M1 Kupffer cells[J]. Journal of Environmental and Occupational Medicine, 2022, 39(1): 65-70. DOI: 10.11836/JEOM21242

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Effect of oral exposure to trichloroethylene on JMJD3 expression and polarization of M1 Kupffer cells

1.
Department of Occupational and Environmental Health, School of Public Health, Anhui Medical University, Hefei, Anhui 230032, China
2.
Institute of Dermatology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, China

Funds: This study was funded.

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Corresponding author:
ZHANG Jiaxiang,Email:zhangjiaxiang@ahmu.edu.cn

ZHU Qixing,Email:zqxing@yeah.net
Received Date: May 23, 2021
Accepted Date: November 14, 2021
Published Date: January 24, 2022

Graphical Abstract

Abstract

Abstract

[Background] Trichloroethylene (TCE) can enter human body through biological accumulation of polluted water or air, resulting in health hazards. The most commonly involved organs are the liver.

[Objective] To observe potential polarization of M1 Kupffer cells (KCs) in mice liver exposed to TCE orally, and to investigate the relationship between histones lysin demethylase JMJD3 and M1 KCs polarization.

[Methods] A total of 72 SPF BALB/c mice aged 6 to 8 weeks were randomly divided into a blank control group (n=18), a vehicle control group (n=18), a 2.5 mg·mL⁻¹ TCE group (n=18), and a 5.0 mg·mL⁻¹ TCE group (n=18) after adaptive feed for one week. A TCE transoral exposure model was established after eight weeks of administration according to previous research of the research group. In the 2nd, 4th, and 8th weeks, the mice were sacrificed and liver tissue samples were collected. Western blotting was used to detect the expression level of JMJD3 in the liver tissue samples. Immunofluorescence was used to co-locate the macrophage marker F4/80 and the surface marker CD11c of M1 macrophages. Immunohistochemistry was used to detect the expressions of CD16/32, a marker of M1 macrophages, and TNF-α, an inflammatory factor of M1 macrophages in mouse liver.

[Results] In the 2nd, 4th, and 8th weeks, the mice in each group were generally in good condition, and no individual died due to TCE. There was no statistically significant difference in the amount of water consumed by each group, nor in the body weight gain and the liver coefficient of mice at each time point (P>0.05). The results of Western blotting analysis showed that there was no statistically significant difference in JMJD3 protein expression level between the blank control group and the vehicle control group at each time point, the expression levels of JMJD3 protein in the 2.5 mg·mL⁻¹ TCE group and the 5.0 mg·mL⁻¹ TCE group were higher than that in the control group , and the expression level of JMJD3 protein in the 5.0 mg·mL⁻¹ TCE group was higher than that in the 2.5 mg·mL⁻¹ TCE group (P<0.05). The results of immunofluorescence co-localization showed that the expressions of F4/80 and CD11c were low in the blank control group and the vehicle control group, while the expressions of F4/80 and CD11c were increased in the 2.5 mg·mL⁻¹ and the 5.0 mg·mL⁻¹ TCE groups. The results of immunohistochemistry showed that the expressions of CD16/32 and TNF-α in the blank control group and the vehicle control group were low, and there were large deposits in the 2.5 mg·mL⁻¹ TCE group and the 5.0 mg·mL⁻¹ TCE group.

[Conclusion] The polarization of M1 KCs and the expression of proinflammatory factors may be related to an increased expression level of JMJD3 induced by oral TCE exposure.
- trichloroethylene,
- liver toxicity,
- Kupffer cell,
- histone lysine demethylase

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References (23)

References

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