288 Se deficiency aggravates AFB1-induced immunotoxicity in chick spleen via regulating six selenoprotein and redox/inflammation/apoptotic signaling

Abstract

Abstract This study was designed to reveal the underlying mechanism of Se-mediated protection against aflatoxin B1 (AFB1)-induced splenic injury in broilers. Four groups of day-old Cobb male broilers (n = 5 cages/diet, 6 chicks/cage) were arranged in a 3-wk 2×2 factorial design trial that fed a Se-deficient, corn and soy–based diet (BD, 36 μg Se/kg) or the BD + 1.0 mg AFB1/kg, 0.3 mg Se/kg, or 1.0 mg AFB1/kg with 0.3 mg Se/kg (as 2-hydroxy-4-methylselenobutanoic acid). Serum and spleen were collected at wk 3 to assay for histology, cytokines, redox status, and selected inflammation- and apoptosis-related genes and proteins, and selenogenome. Dietary AFB1 induced the growth retardation and spleen injury, decreasing (P < 0.05) body weight gain, feed intake, feed conversion efficiency, and serum interleukin-1β, increasing (P < 0.05) spleen index and serum interleukin-6, and reduced the splenic lymphocyte number and white pulp region and histiocyte proliferation in Se adequate groups. However, Se deficiency aggravated (P < 0.05) these AFB1-induced changes. Moreover, Se deficiency decreased (P < 0.05) splenic glutathione peroxidases (GPX) activities and glutathione concentration in AFB1 exposed groups. Furthermore, Se deficiency also upregulated (P < 0.05) the antimicrobial (beta defensin 1 and 2) and apoptotic (Caspase 3 and Caspase 9) genes but downregulated (P < 0.05) antiapoptotic (B-cell lymphoma 2) and inflammatory (E3 ubiquitin-protein ligase CBL-B) genes at mRNA and(or) protein levels in AFB1 supplementation groups. Additionally, Se deficiency downregulated (P < 0.05) GPX3, thioredoxin reductase 1 (TXNRD 1), GPX4 and selenoprotein (SELENO) S and upregulated (P < 0.05) SELENOT and SELENOU in spleen in AFB1 administered groups. In conclusions, dietary Se deficiency aggravated AFB1-induced spleen injury in chicks, partially through the regulation of the oxidative stress, inflammatory and apoptotic signaling and six selenoproteins (Supported in part by Chinese Natural Science Foundation Projects 31772636 and 31501987).