Increased levels of IL-6, IL-1β, and TNF-α in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency

Rheumatol Int. 2014 Jul;34(7):995-1004. doi: 10.1007/s00296-013-2862-5. Epub 2013 Sep 15.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cartilage, Articular / immunology
  • Cartilage, Articular / pathology
  • Child
  • Disease Models, Animal
  • Female
  • Finger Phalanges / immunology
  • Finger Phalanges / pathology
  • Gene Expression / immunology
  • Humans
  • Interleukin-1beta / blood
  • Interleukin-1beta / genetics
  • Interleukin-1beta / immunology*
  • Interleukin-6 / blood
  • Interleukin-6 / genetics
  • Interleukin-6 / immunology*
  • Kashin-Beck Disease / complications
  • Kashin-Beck Disease / immunology*
  • Kashin-Beck Disease / pathology
  • Knee Joint / immunology
  • Knee Joint / pathology
  • Male
  • Rats, Sprague-Dawley
  • Selenium / deficiency*
  • T-2 Toxin / toxicity*
  • Tumor Necrosis Factor-alpha / blood
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / immunology*


  • IL1B protein, human
  • IL1B protein, rat
  • IL6 protein, human
  • Interleukin-1beta
  • Interleukin-6
  • Tumor Necrosis Factor-alpha
  • Selenium
  • T-2 Toxin