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Comparative and combined effects of interleukin-6, interleukin-1β, and tumor necrosis factor α on proteoglycan metabolism of human articular chondrocytes cultured in agarose

(1994) JOURNAL OF RHEUMATOLOGY. 21(2). p.314-320
Author
Organization
Abstract
Objective. To study the effects of recombinant tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta) and interleukin 6 (IL-6) on proteoglycan metabolism of isolated chondrocytes. Methods. Human articular cartilage cells were cultured in agarose gel. In these culture conditions, chondrocytes keep their phenotypic stability. They release cartilage specific proteoglycans into the surrounding artificial matrix. Proteoglycan synthesis was measured by the incorporation of (35)sulfate (S-35). Results. TNF-alpha and IL-1 beta depressed proteoglycan synthesis and induced proteoglycan degradation. The effects of both cytokines were additive, when used in submaximal doses. No mutual induction of TNF-alpha and IL-1 beta was shown, but both cytokines stimulated the chondrocytes to release IL-6, up to 100,000 pg/ml. Equal amounts of human recombinant IL-6 did not affect proteoglycan synthesis. IL-6 did not alter proteoglycan quality, nor did it modulate the IL-1 beta activities on proteoglycan metabolism. Conclusion. These findings illustrate the role of IL-1 beta and TNF-alpha in cartilage degradation and suggest that the role of the large amounts of IL-6 released in response to IL-1 in chronic arthritis is not directly protective with regard to proteoglycan metabolism.
Keywords
CYTOKINES, CARTILAGE, INVITRO, MODULATION, INFLAMMATION, INHIBITOR, TNF-ALPHA, ELECTRON-MICROSCOPY, RHEUMATOID-ARTHRITIS, :ARTHRITIS SYNOVIAL-FLUID, PROTEOGLYCAN METABOLISM, TUMOR NECROSIS FACTOR ALPHA, HUMAN CHONDROCYTE, INTERLEUKIN 1-BETA, INTERLEUKIN 6

Citation

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Chicago
Malfait, Anne-Marie, August Verbruggen, Eric Veys, J Lambert, Leo De Ridder, and Maria Cornelissen. 1994. “Comparative and Combined Effects of Interleukin-6, Interleukin-1β, and Tumor Necrosis Factor α on Proteoglycan Metabolism of Human Articular Chondrocytes Cultured in Agarose.” Journal of Rheumatology 21 (2): 314–320.
APA
Malfait, A.-M., Verbruggen, A., Veys, E., Lambert, J., De Ridder, L., & Cornelissen, M. (1994). Comparative and combined effects of interleukin-6, interleukin-1β, and tumor necrosis factor α on proteoglycan metabolism of human articular chondrocytes cultured in agarose. JOURNAL OF RHEUMATOLOGY, 21(2), 314–320.
Vancouver
1.
Malfait A-M, Verbruggen A, Veys E, Lambert J, De Ridder L, Cornelissen M. Comparative and combined effects of interleukin-6, interleukin-1β, and tumor necrosis factor α on proteoglycan metabolism of human articular chondrocytes cultured in agarose. JOURNAL OF RHEUMATOLOGY. 1994;21(2):314–20.
MLA
Malfait, Anne-Marie, August Verbruggen, Eric Veys, et al. “Comparative and Combined Effects of Interleukin-6, Interleukin-1β, and Tumor Necrosis Factor α on Proteoglycan Metabolism of Human Articular Chondrocytes Cultured in Agarose.” JOURNAL OF RHEUMATOLOGY 21.2 (1994): 314–320. Print.
@article{196886,
  abstract     = {Objective. To study the effects of recombinant tumor necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta) and interleukin 6 (IL-6) on proteoglycan metabolism of isolated chondrocytes. 
Methods. Human articular cartilage cells were cultured in agarose gel. In these culture conditions, chondrocytes keep their phenotypic stability. They release cartilage specific proteoglycans into the surrounding artificial matrix. Proteoglycan synthesis was measured by the incorporation of (35)sulfate (S-35). 
Results. TNF-alpha and IL-1 beta depressed proteoglycan synthesis and induced proteoglycan degradation. The effects of both cytokines were additive, when used in submaximal doses. No mutual induction of TNF-alpha and IL-1 beta was shown, but both cytokines stimulated the chondrocytes to release IL-6, up to 100,000 pg/ml. Equal amounts of human recombinant IL-6 did not affect proteoglycan synthesis. IL-6 did not alter proteoglycan quality, nor did it modulate the IL-1 beta activities on proteoglycan metabolism. 
Conclusion. These findings illustrate the role of IL-1 beta and TNF-alpha in cartilage degradation and suggest that the role of the large amounts of IL-6 released in response to IL-1 in chronic arthritis is not directly protective with regard to proteoglycan metabolism.},
  author       = {Malfait, Anne-Marie and Verbruggen, August and Veys, Eric and Lambert, J and De Ridder, Leo and Cornelissen, Maria},
  issn         = {0315-162X},
  journal      = {JOURNAL OF RHEUMATOLOGY},
  keyword      = {CYTOKINES,CARTILAGE,INVITRO,MODULATION,INFLAMMATION,INHIBITOR,TNF-ALPHA,ELECTRON-MICROSCOPY,RHEUMATOID-ARTHRITIS,:ARTHRITIS SYNOVIAL-FLUID,PROTEOGLYCAN METABOLISM,TUMOR NECROSIS FACTOR ALPHA,HUMAN CHONDROCYTE,INTERLEUKIN 1-BETA,INTERLEUKIN 6},
  language     = {eng},
  number       = {2},
  pages        = {314--320},
  title        = {Comparative and combined effects of interleukin-6, interleukin-1\ensuremath{\beta}, and tumor necrosis factor \ensuremath{\alpha} on proteoglycan metabolism of human articular chondrocytes cultured in agarose},
  volume       = {21},
  year         = {1994},
}