Measurement of the bioactivity of interleukin and tumour necrosis factor in synovial fluid of Kashin-Beck disease

Abstract

We studied the bioactivity of interleukin-1 (IL-1) and tumour necrosis factor (TNF) in the synovial fluid of 12 patients with Kashin-Beck disease (KBD), 8 patients with osteoarthritis (OA) and 8 normal controls. C57 female mouse T cell proliferation method was used to test the bioactivity of IL-1, and lethality method with L929 cells to test the bioactivity of TNF. The bioactivities of IL-1 and TNF in the synovial fluid from patients with KBD were higher than those in the synovial fluid of osteoarthritis and normal controls, indicating the participation of IL-1 and TNF in the pathogenesis of KBD.Résumé Nous avons étudié la bioactivité de l'interleukin-1 (IL-1) et du facteur de nécrose tumorale (TNF) dans le liquide synovial de 12 patients atteints de la maladie de Kashin-Beck (KBD), 8 patients d'arthrose et 8 sujets té-moins. La bioactivité de IL-1 est évaluée par la méthode de prolifération des cellules T de souris femelles C57 et le TNF par la mortalité des cellules L929. L'activité d'IL-1 et de TNF dans le liquide synovial des patients atteints de KBD est plus élevée que pour l'arthrose et les sujets normaux, révélant la participation d'IL-1 et de TNF dans la pathogenèse de la maladie de Kashin-Beck.

Proteoglycan metabolism, cell death and Kashin-Beck Disease

“…It has been reported that T-2 toxin significantly inhibited aggrecan gene and protein expression in chondrocytes cultured in vitro [52, 57], but increased the corresponding gene expression of degradative enzymes such as aggrecanase-2 [57]. Moreover, mycotoxins can increase the production of pro-inflammatory cytokines such as IL-1β and TNF-α in vitro [58, 59] and in vivo [60], similar to their elevated levels reported in KBD patients [2, 14, 16, 17, 61, 62]. These increased levels of pro-inflammatory cytokines could undoubtedly promote the catabolism of PGs in the ECM of articular cartilage.…”

Role of inflammation in the process of clinical Kashin-Beck disease: latest findings and interpretations

“…Some early studies in KBD with the comparisons of RA and OA tissues, observed dramatically increased levels of inflammatory cytokines and proteins in KBD tissues [4,[18][19][20][21]. Although the inflammatory expression was largely overshadowed by more pronounced histological and biochemical abnormalities in RA and OA, elevated levels of inflammatory cytokines and proteins in both the serum and synovial fluid of patients with KBD were reported early this century [4][5][6][7][8][9][10]; from then on, more and more reports data of the inflammatory studies on KBD were provided. Unfortunately, because of the common use of RA and OA tissues and fluids as comparators in KBD investigations, the inflammatory effect of KBD has been underestimated.…”

“…However, 20 years ago, the synovial inflammation in KBD patients was observed [3]. Subsequently, the inflammatory cytokines in articular synovial fluid [4][5][6] and serum [7][8][9][10] from KBD patients were investigated. Given greater appreciation for inflammatory response in patients with KBD, inflammation has been highly emphasized in the study of KBD progression recently.…”

Association of TNF-α and Fas gene promoter polymorphism with the risk of Kashin–Beck disease in Northwest Chinese population

“…have been detected in the serum and synovial fluid of KBD [7][8][9], and showed higher levels and expression both serum and cartilage in KBD patient contrast to the healthy controls [5][6][7]. Meanwhile, excessive apoptosis and dedifferentiation of chondrocytes with focus chondronecrosis were also observed in KBD growth plate and articular cartilage [10,11].…”