Selenium Deficiency Activates Heat Shock Protein Expression in Chicken Spleen and Thymus

Heat shock proteins (Hsps) are protective proteins present in nearly all species; they are used as biomarkers of various stress conditions in humans, animals, and birds. Selenium (Se) deficiency, which can depress the production of Hsps, can cause chicken tissue injuries. To investigate Hsp production, mRNA, and protein levels in Se-deficient chicken spleens and thymuses, a total of 180 1-day-old sea blue white laying hens (90 chickens/group) were harvested in two groups (the control group and the Se-deficient group) in 15, 25, 35, 45, and 55 days, respectively. The results showed that mRNA levels of Hsp27, Hsp40, Hsp60, Hsp70, and Hsp90 were significantly increased in the spleens and thymuses of the Se-deficient group compared to the control group. Further protein levels of Hsp60, Hsp70, and Hsp90 were also significantly increased in the spleen and thymus of the Se-deficient group compared to the control group. Meanwhile, the spleen expression ratio of Hsp40 mRNA level and Hsp70 protein level were higher in the Se-deficient group than other proteins. In the thymus, the Hsp90 mRNA level and Hsp60 protein expression level were the highest level in the Se-deficient group among other proteins. Based on these results, we concluded that Se deficiency could induce a protective stress response in chicken by means of promoting the mRNA and protein expression of Hsps, thus easing the effects of Se deficiency to some extent.