Anorexia induction by the deoxynivalenol (vomitoxin) is mediated by proinflammatory cytokines

• 作 者: WU Wenda ZHANG Haibin
• 机 构: College of Veterinary Medicine, Nanjing Agricultural University,Nanjing 210095 ,P.R.China
• 出 处: 中国畜牧兽医学会兽医内科与临床诊疗学分会第八届代表大会暨学术研讨会
• 发表日期: 2015年4期
• 关键词: mycotoxin trichothecene anorexia deoxynivalenol TNF-α IL-1β

　　The trichothecene deoxynivalenol (DON), a foodborne mycotoxin found in grain-based foods, has been associated with human and animal food poisoning.Although induction of anorexia has been described as a hallmark of DON-induced toxicity in many animal species, the mechanistic basis for this adverse effect is not fully understood.The purpose of this research was to determine the role of two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in DON-induced anorexia.In a nocturnal mouse food consumption model, DON-induced anorectic response occurred at 1 h and lasted up to 6 h.Similar anorectic effects were observed following acute administration of exogenous TNF-α and IL-1β.Oral exposure to DON at 5 mg/(kg ·BW) stimulated splenic and hepatic mRNA and plasma protein elevations of TNF-α and IL-1β that corresponded to anorexia induction.Pretreatment with the TNF-α receptor (TNFR) antagonist R-7050 dose-dependently attenuated both TNF-α-and DON-induced anorexia.While, the type 1 IL-1 receptor (IL-1R1) antagonist IL-1RA dose-dependently attenuated both IL-1 β-and DON-induced anorexia.Taken together, the results suggest that both TNF-α and IL-1β play contributory role in anorexia induction following oral exposure to DON.