Antagonistic effect of selenium on mercuric chloride in the central immune organs of chickens: The role of microRNA‐183/135b‐FOXO1/TXNIP/NLRP3 inflammasome axis

Mercury (Hg) is a persistent environmental and industrial pollutant that accumulated in the body and induces oxidative stress and inflammation damage. Selenium (Se) has been reported to antagonize immune organs damage caused by heavy metals. Here, we aimed to investigate the prevent effect of Se on...

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Bibliographic Details
Published in:Environmental toxicology 2022-05, Vol.37 (5), p.1047-1057
Main Authors: Gao, Pei‐Chao, Chen, Xue‐Wei, Chu, Jia‐Hong, Li, Lan‐Xin, Wang, Zhen‐Yong, Fan, Rui‐Feng
Format: Article
Language:English
Subjects:
Body organs
Bursa of Fabricius
central immune organ
Chickens
Chlorides
Cytokines
Damage accumulation
Forkhead protein
FOXO1 protein
FOXO1/TXNIP/NLRP3 inflammasome
Heavy metals
Immunosuppression
Industrial pollution
Inflammasomes
Inflammation
Lymphocytes
Mercuric chloride
Mercury
Mercury (metal)
Mercury compounds
Metals
microRNA
MicroRNAs
miRNA
Organs
Oxidative stress
Peripheral blood
Pollutants
Pyrin protein
Receptors
Ribonucleic acid
RNA
Selenium
Thioredoxin
Thymus
Thymus gland
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Summary:Mercury (Hg) is a persistent environmental and industrial pollutant that accumulated in the body and induces oxidative stress and inflammation damage. Selenium (Se) has been reported to antagonize immune organs damage caused by heavy metals. Here, we aimed to investigate the prevent effect of Se on mercuric chloride (HgCl2)‐induced thymus and bursa of Fabricius (BF) damage in chickens. The results showed that HgCl2 caused immunosuppression by reducing the relative weight, cortical area of the thymus and BF, and the number of peripheral blood lymphocytes. Meanwhile, HgCl2 induced oxidative stress and imbalance in cytokines expression in the thymus and BF. Further, we found that thioredoxin‐interacting protein (TXNIP) and the NOD‐like receptor pyrin domain containing 3 (NLRP3) inflammasome mediated HgCl2‐induced oxidative stress and inflammation. Mechanically, the targeting and inhibitory effect of microRNA (miR)‐135b/183 on forkhead box O1 (FOXO1) were an upstream event for HgCl2‐activated TXNIP/NLRP3 inflammasome pathway. Most importantly, Se effectively attenuated the aforementioned damage in the thymus and BF caused by HgCl2 and inhibited the TXNIP/NLRP3 inflammasome pathway by reversing the expression of FOXO1 through inhibiting miR‐135b/183. In conclusion, the miR‐135b/183‐FOXO1/TXNIP/NLRP3 inflammasome axis might be a novel mechanism for Se to antagonize HgCl2‐induced oxidative stress and inflammation in the central immune organs of chickens.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.23463