Chemokine production by human chondrocytes

Lia Pulsatelli, Paolo Dolzani, Anna Piacentini, Tania Silvestri, Romina Ruggeri, Gualtiero Gualtieri, Riccardo Meliconi, Andrea Facchini

Research output: Contribution to journalArticle

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Abstract

Objective. To evaluate the role of chondrocytes in producing CXC chemokines [interleukin 8 (IL-8), growth related gene product (GRO-α)] and CC chemokines [monocyte chemoattractant protein (MCP- 1), macrophage inflammatory protein (MIP-1α), RANTES] in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and subjects after traumatic injury (PT). Methods. Articular cartilage specimens were obtained from 38 patients with OA and 18 with RA under- going joint replacement surgery. Healthy human cartilage was obtained from femoral condyles removed after trauma in 11 subjects with no history of joint pathology (PT cases). Chondrocytes were isolated from articular cartilage by sequential enzymatic digestion and cultured in vitro. Chemokine production was investigated in unstimulated condition and after 72 h incubation with proinflammatory [IL-1β, tumor necrosis factor-α (TNF-α)] and antiinflammatory [transforming growth factor-β1 (TGF-β1), IL-l0] mediators. Chemokine concentrations in cell supernatants were evaluated by ELISA. Results. Chondrocytes produce all these chemokines to a different extent. IL-1β was a more potent stimulus than TNF- α in inducing production of all chemokines except MCP-1. We found no statistical differences among chondrocytes isolated from OA, RA, and PT for chemokine production in either basal conditions or after cytokine stimulation. IL-1β induced chemokine production can be modulated by TGF-β1 in different ways according to the various chemokines, while IL-10 does not affect IL-1β induced chemokine production. Conclusion. Chondrocytes produce IL-8, GRO-α, MCP-1, MIP-1α, and RANTES. Proinflammatory factors (IL-1β, TNF-α) effectively upregulate chemokine production, but production is scarcely modulated by the antiinflammatory mediators TGF-β and IL-10. Chondrocyte derived chemokines may play a role in triggering the mechanisms involved in pathogenesis and persistence of joint diseases.

Original languageEnglish
Pages (from-to)1992-2001
Number of pages10
JournalJournal of Rheumatology
Volume26
Issue number9
Publication statusPublished - 1999

Fingerprint

Chondrocytes
Chemokines
Interleukin-1
Osteoarthritis
Chemokine CCL5
Rheumatoid Arthritis
Tumor Necrosis Factor-alpha
Articular Cartilage
Transforming Growth Factors
Interleukin-8
Interleukin-10
Replacement Arthroplasties
Anti-Inflammatory Agents
Macrophage Inflammatory Proteins
CXC Chemokines
CC Chemokines
Joint Diseases
Chemokine CCL2
Wounds and Injuries
Thigh

Keywords

  • Arthritis
  • Chemokines
  • Chondrocytes

ASJC Scopus subject areas

  • Rheumatology
  • Immunology

Cite this

Pulsatelli, L., Dolzani, P., Piacentini, A., Silvestri, T., Ruggeri, R., Gualtieri, G., ... Facchini, A. (1999). Chemokine production by human chondrocytes. Journal of Rheumatology, 26(9), 1992-2001.

Chemokine production by human chondrocytes. / Pulsatelli, Lia; Dolzani, Paolo; Piacentini, Anna; Silvestri, Tania; Ruggeri, Romina; Gualtieri, Gualtiero; Meliconi, Riccardo; Facchini, Andrea.

In: Journal of Rheumatology, Vol. 26, No. 9, 1999, p. 1992-2001.

Research output: Contribution to journalArticle

Pulsatelli, L, Dolzani, P, Piacentini, A, Silvestri, T, Ruggeri, R, Gualtieri, G, Meliconi, R & Facchini, A 1999, 'Chemokine production by human chondrocytes', Journal of Rheumatology, vol. 26, no. 9, pp. 1992-2001.
Pulsatelli L, Dolzani P, Piacentini A, Silvestri T, Ruggeri R, Gualtieri G et al. Chemokine production by human chondrocytes. Journal of Rheumatology. 1999;26(9):1992-2001.
Pulsatelli, Lia ; Dolzani, Paolo ; Piacentini, Anna ; Silvestri, Tania ; Ruggeri, Romina ; Gualtieri, Gualtiero ; Meliconi, Riccardo ; Facchini, Andrea. / Chemokine production by human chondrocytes. In: Journal of Rheumatology. 1999 ; Vol. 26, No. 9. pp. 1992-2001.
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abstract = "Objective. To evaluate the role of chondrocytes in producing CXC chemokines [interleukin 8 (IL-8), growth related gene product (GRO-α)] and CC chemokines [monocyte chemoattractant protein (MCP- 1), macrophage inflammatory protein (MIP-1α), RANTES] in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and subjects after traumatic injury (PT). Methods. Articular cartilage specimens were obtained from 38 patients with OA and 18 with RA under- going joint replacement surgery. Healthy human cartilage was obtained from femoral condyles removed after trauma in 11 subjects with no history of joint pathology (PT cases). Chondrocytes were isolated from articular cartilage by sequential enzymatic digestion and cultured in vitro. Chemokine production was investigated in unstimulated condition and after 72 h incubation with proinflammatory [IL-1β, tumor necrosis factor-α (TNF-α)] and antiinflammatory [transforming growth factor-β1 (TGF-β1), IL-l0] mediators. Chemokine concentrations in cell supernatants were evaluated by ELISA. Results. Chondrocytes produce all these chemokines to a different extent. IL-1β was a more potent stimulus than TNF- α in inducing production of all chemokines except MCP-1. We found no statistical differences among chondrocytes isolated from OA, RA, and PT for chemokine production in either basal conditions or after cytokine stimulation. IL-1β induced chemokine production can be modulated by TGF-β1 in different ways according to the various chemokines, while IL-10 does not affect IL-1β induced chemokine production. Conclusion. Chondrocytes produce IL-8, GRO-α, MCP-1, MIP-1α, and RANTES. Proinflammatory factors (IL-1β, TNF-α) effectively upregulate chemokine production, but production is scarcely modulated by the antiinflammatory mediators TGF-β and IL-10. Chondrocyte derived chemokines may play a role in triggering the mechanisms involved in pathogenesis and persistence of joint diseases.",
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AU - Pulsatelli, Lia

AU - Dolzani, Paolo

AU - Piacentini, Anna

AU - Silvestri, Tania

AU - Ruggeri, Romina

AU - Gualtieri, Gualtiero

AU - Meliconi, Riccardo

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AB - Objective. To evaluate the role of chondrocytes in producing CXC chemokines [interleukin 8 (IL-8), growth related gene product (GRO-α)] and CC chemokines [monocyte chemoattractant protein (MCP- 1), macrophage inflammatory protein (MIP-1α), RANTES] in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and subjects after traumatic injury (PT). Methods. Articular cartilage specimens were obtained from 38 patients with OA and 18 with RA under- going joint replacement surgery. Healthy human cartilage was obtained from femoral condyles removed after trauma in 11 subjects with no history of joint pathology (PT cases). Chondrocytes were isolated from articular cartilage by sequential enzymatic digestion and cultured in vitro. Chemokine production was investigated in unstimulated condition and after 72 h incubation with proinflammatory [IL-1β, tumor necrosis factor-α (TNF-α)] and antiinflammatory [transforming growth factor-β1 (TGF-β1), IL-l0] mediators. Chemokine concentrations in cell supernatants were evaluated by ELISA. Results. Chondrocytes produce all these chemokines to a different extent. IL-1β was a more potent stimulus than TNF- α in inducing production of all chemokines except MCP-1. We found no statistical differences among chondrocytes isolated from OA, RA, and PT for chemokine production in either basal conditions or after cytokine stimulation. IL-1β induced chemokine production can be modulated by TGF-β1 in different ways according to the various chemokines, while IL-10 does not affect IL-1β induced chemokine production. Conclusion. Chondrocytes produce IL-8, GRO-α, MCP-1, MIP-1α, and RANTES. Proinflammatory factors (IL-1β, TNF-α) effectively upregulate chemokine production, but production is scarcely modulated by the antiinflammatory mediators TGF-β and IL-10. Chondrocyte derived chemokines may play a role in triggering the mechanisms involved in pathogenesis and persistence of joint diseases.

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