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खुला एक्सेस

अमूर्त

Pentraxin-3 and its Association with C1q-CIC, hsCRP and Pro-Inflammatory Cytokines (TNF-Α and IL-1β) among SLE Patients from India

Khadilkar PV, Umare VD, Rajadhyaksha A, Chougule DA, Vaidya SP, Deshpande SD, Nadkarni AH and Pradhan VD

Introduction: Systemic Lupus Erythematosus (SLE) is a prototype autoimmune disease with alternating periods of flares and remission. Disease pathogenesis involves vast inflammatory responses, characterized by impaired cell signaling and T-cell dysfunction with interplay of cytokines and a wide network of protein cascades. Aim of this study is to understand the correlation between PTX-3 and pro-inflammatory cytokines (TNF-α and IL-1β) and their role in disease pathogenesis of SLE.
Materials and Methods: Sixty-three SLE patients classified as per ACR 1997 criteria were included, of which 36 had renal involvement (LN). Autoantibodies were detected by IFA and ANA BLOT techniques. Serum Complement levels and hsCRP (by nephelometer), Pentraxin-3 and C1q-CIC (by ELISA), TNF-α and IL-1β levels (by Multiplex immunoassay) were assessed.
Results: ANA was present in 90.5% patients, anti-dsDNA antibodies were present in 87.3% patients. Reduced C3 (<90 mg/dl) and C4 (<15 mg/dl) levels were found in 58.7% patients. hsCRP was elevated (>5 mg/L) in 49.2% patients. C1q-CIC levels were high (>50 μg/ml) in 50.8% patients. Serum PTX-3 levels and TNF-α levels were significantly higher in SLE patients than healthy controls (p<0.0001 and p<0.0001 respectively). It was observed that PTX-3 and IL-1β levels were significantly higher in LN patients as compared with nonLN patients (p=0.0107; p=0.0022 respectively). PTX-3 positively correlates with C1q-CIC and negatively correlates with hsCRP and IL-1β levels among SLE patients.
Conclusion: This study suggests that serum PTX-3 though do not induce an immediate inflammatory response, its positive correlation with C1q-CIC levels, suggested its possible role in classical complement pathway activation. Further studies in this regard are needed to understand the role of PTX-3 in pathogenesis of SLE.