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FRI0500 Evaluation of the Role of Fractalkine Chemokine CX3CL1 and Its Receptor CX3CR1 in Inflammatory Myopathies
  1. S. Colafrancesco1,
  2. R. Priori1,
  3. E. Astorri1,
  4. R. Scrivo1,
  5. G. D'Amati2,
  6. C. Giordano2,
  7. G. Valesini1
  1. 1Dipartimento di Medicina Interna e Specialità Mediche
  2. 2Dipartimento di Scienze Radiologiche, Oncologiche ed Anatomopatologiche, Sapienza Università di Roma, Rome, Italy


Background In inflammatory myopathies (IM), including polymyositis (PM), dermatomyositis (DM) and inclusion body myositis (IBM), serum creatinine kinase (CKs) can be not always reliable to evaluate disease activity. Thus, new biomarkers are required. CX3CL1/fractalkine seems to be expressed on the infiltrated inflammatory cells in muscle of murine model of experimental autoimmune myositis. Since cytotoxic T cells and macrophages invade muscle tissue in IM, interaction between CX3CL1 and its receptor (CX3CR1) may contribute to cells migration. An increased serum and tissue expression of CX3CL1 and CX3CR1 in Sjogren's Syndrome (SS) and Rheumatoid Arthritis has been already detected confirming the involvement of this chemokine in the recruitment of inflammatory cells in the target organs.

Objectives To evaluate the CX3CL1 expression in sera and muscle biopsies from a large cohort of patients with IM and to correlate its expression with CKs levels.

Methods Seventy four patients attending our Rheumatology Unit were enrolled. CX3CL1 serum levels were evaluated by a Human CX3CL1/Fractalkine Quantikine ELISA kit (R&D Systems) in: 19 patients with IM; as positive control 5 patients with a secondary inflammatory myopathy (2nd IM) (3 SS and 2 Systemic Sclerosis) and 40 SS; as negative control 2 patients with rhabdomyolisis not related to an autoimmune inflammatory condition (no-IM) and 4 patients with Systemic Lupus Erythematosus (SLE). In all patients, anti-nuclear (ANA) and anti-extractable nuclear antigens (ENA) antibodies and CKs were detected. Staining for CX3CL1 and CX3CR1 were performed on sequential paraffin mounted sections of muscle biopsies from 2 patients with IM. Tonsil tissue was used as positive control.

Results Clinical and serological characteristics of the enrolled patients are reported in table. Mean CX3CL1 serum level in patients with IM was 1.29±0.9 ng/ml. Mean CX3CL1 serum level in positive control groups was: 1.5±0.68 ng/ml in 2nd IM and 1.03±0.4 ng/ml in SS. In the negative control groups was: 0.58±0.07 ng/ml in no-IM and 0.65±0.06 ng/ml in SLE patients. CX3CL1 serum levels were significantly higher in IM or 2nd IM compared to no-IM (p<0.003). In all patients with rhabdomyolisis (IM, 2nd IM, no-IM) CX3CL1 serum levels correlated with CKs (p=0.028, r=0.43). Hystological evaluation of CX3CL1 and CX3CR1 staining on sequential muscle biopsies showed lymphocytes expressing both markers.

Table 1

Conclusions In course of IM the serum levels of CX3CL1 are increased and comparable to the positive control. This chemokine positively correlates with rhabdomyolisis and its serum level is significantly increased in patients with IM compared to patients with no-IM. Both CX3CL1 and CX3CR1 are detectable at tissue level confirming an active role of the chemokines in the inflammatory process.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.4128

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