title: Increased levels of IL-6, IL-1β, and TNF-α in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency.
abstract: The objective of this study is to investigate the possible role of inflammatory mediators such as IL-6, IL-1β, and TNF-α in Kashin-Beck disease (KBD) children and rats fed with T-2 toxin under a selenium-deficient nutrition status in order to determine possible mechanism underlying KBD. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. The morphology of joint cartilages of KBD children and rats was examined by light microscopy, and the expression of proteoglycans was determined by histochemical staining. The serum levels of IL-6, IL-1β, and TNF-α were determined by enzyme-linked immunosorbent assay. IL-6, IL-1β and TNF-α were localized by immunohistochemistry, and their mRNA levels were detected by real-time RT-PCR. The serum levels of IL-6 were significantly elevated in rats fed with selenium-deficient, T-2 toxin, and T-2 toxin plus selenium-deficient diets compared to those in the normal diet, while the serum levels of IL-1β and TNF-α were significantly increased only in the T-2 toxin plus selenium-deficient diet group. IL-6, IL-1β and TNF-α protein and mRNA levels in cartilage were significantly higher in rats with diets of T-2 toxin and T-2 toxin plus selenium deficiency than in rats fed normal or selenium-deficient diet. While staining for the cytokines in cartilages of KBD children was significantly higher than that in controls. T-2 toxin under a selenium-deficient nutritional status induces increased levels of IL-6, IL-1β, and TNF-α in serum and cartilages, which may account for the pathological mechanism underlying the cartilage damage in KBD.
authors.affiliation: Institute of Endemic Diseases, Xi'an Jiaotong University College of Medicine, Xi'an, 710061, Shaanxi, People's Republic of China.
authors.forename: Xiaorong
authors.initials: X
authors.lastname: Zhou
authors.forename: Zhilun
authors.initials: Z
authors.lastname: Wang
authors.forename: Jinghong
authors.initials: J
authors.lastname: Chen
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Daiqing
authors.initials: D
authors.lastname: Song
authors.forename: Siyuan
authors.initials: S
authors.lastname: Li
authors.forename: Haojie
authors.initials: H
authors.lastname: Yang
authors.forename: Senhai
authors.initials: S
authors.lastname: Xue
authors.forename: Chen
authors.initials: C
authors.lastname: Chen
mesh_terms: D000818:Animals; D002358:Cartilage, Articular / Q000276:immunology / Q000473:pathology; D002648:Child; D004195:Disease Models, Animal; D005260:Female; D050278:Finger Phalanges / Q000276:immunology / Q000473:pathology; D015870:Gene Expression / Q000276:immunology; D006801:Humans; D053583:Interleukin-1beta / Q000097:blood / Q000235:genetics / Q000276:immunology*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics / Q000276:immunology*; D057767:Kashin-Beck Disease / Q000150:complications / Q000276:immunology* / Q000473:pathology; D007719:Knee Joint / Q000276:immunology / Q000473:pathology; D008297:Male; D017207:Rats, Sprague-Dawley; D012643:Selenium / Q000172:deficiency*; D013605:T-2 Toxin / Q000633:toxicity*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics / Q000276:immunology*
chemical_list: C508585:IL1B protein, human; C000594089:IL1B protein, rat; C508600:IL6 protein, human; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D012643:Selenium; D013605:T-2 Toxin
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