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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 (HgCl 2 )-induced thymus and bursa of Fabricius (BF) damage in chickens. The results showed that HgCl 2 caused immunosuppression by reducing the relative weight, cortical area of the thymus and BF, and the number of peripheral blood lymphocytes. Meanwhile, HgCl 2 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 HgCl 2 -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 HgCl 2 -activated TXNIP/NLRP3 inflammasome pathway. Most importantly, Se effectively attenuated the aforementioned damage in the thymus and BF caused by HgCl 2 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 HgCl 2 -induced oxidative stress and inflammation in the central immune organs of chickens. K E Y W O R D S central immune organ, FOXO1/TXNIP/NLRP3 inflammasome, mercuric chloride, microRNA, selenium | INTRODUCTIONMercury (Hg) is a toxic heavy metal that is not essential for life but widely distributed in the environment. A series of Hg pollution accidents, such as the Minamata incident in Japan and the contaminated wheat grain incident in Iraq, prompted the signing of the Minamata Convention to limit the use and release of Hg. 1 Due to small-scale gold mining, coal burning, and irrational use of agricultural chemicals have not been eliminated, residents and animals in some countries and regions are still threatened by the high risk of Hg exposure. 2,3 Epidemiological investigations have shown that Hg exposure could induce oxidative stress, inflammation, and dysfunction in tissues 4,5 and cells. 6 The immune organs are responsible for immune cell generation, differentiation, and settlement and are essential for innate and