Effect of Proinflammatory Cytokines (IL-6, TNF-α, and IL-1β) on Clinical Manifestations in Indian SLE Patients

Systemic lupus erythematosus (SLE) is an inflammatory rheumatic disease characterized by production of autoantibodies and organ damage. Elevated levels of cytokines have been reported in SLE patients. In this study we have investigated the effect of proinflammatory cytokines (IL-6, TNF-α, and IL-1β) on clinical manifestations in 145 Indian SLE patients. One hundred and forty-five healthy controls of the same ethnicity served as a control group. Clinical disease activity was scored according to SLEDAI score. Accordingly, 110 patients had active disease and 35 patients had inactive disease. Mean levels of IL-6, TNF-α, and IL-1β were found to be significantly higher in SLE patients than healthy controls (P<0.001). Mean level of IL-6 for patients with active disease (70.45±68.32 pg/mL) was significantly higher (P=0.0430) than those of inactive disease patients (43.85±63.36 pg/mL). Mean level of TNF-α was 44.76±68.32 pg/mL for patients with active disease while it was 25.97±22.03 pg/mL for those with inactive disease and this difference was statistically significant (P=0.0161). Similar results were obtained for IL-1β (P=0.0002). Correlation between IL-6, TNF-α, and IL-1β serum levels and SLEDAI score was observed (r=0.20, r=0.27, and r=0.38, resp.). This study supports the role of these proinflammatory cytokines as inflammatory mediators in active stage of disease

Analysis of Complement Receptor Type 1 (CR1) Polymorphisms and Its Association With Malaria in Rural Population of Maharashtra

The interaction between human host and the Plasmodium parasite is complex. The factors affecting the causality of infection and its severity are yet not completely understood. Single Nucleotide Polymorphisms (SNP) associated with CR1 may be associated with patho-physiology of malaria and its susceptibility to the disease. Methods: The objective of the present study was to calculate the incidence of various antigens of Knops blood group system and CR1 Exon22 polymorphisms in rural population from Chiplun Taluka of Ratnagiri district. The study included 112 malaria positive cases and 909 healthy controls, which were screened for CR1 Exon22 polymorphism. Knops (Kna/b), McCoy (McCa/b), Swain-Langley (Sl1/2) polymorphisms were screened in 93 cases and 321 healthy controls. The frequencies were determined using a PCR-RFLP technique. Results: Only wild types of the allele form were observed in Knops blood group system in malaria cases and healthy control. CR1 exon22 polymorphism was seen in the study population with all the 3 allele type distributed in the cases and control samples. No significant allelic or genotypic differences were found between the controls and the disease groups. Conclusion: The results of the present study demonstrate that common CR1 Exon22 and Knops blood group system are not associated with malaria in the endemic area

The Fc Receptor Polymorphisms and Expression of Neutrophil Activation Markers in Patients with Sickle Cell Disease from Western India

Objective. Sickle cell disease has variable clinical manifestations. Activation of neutrophils plays an important role in the initiation and propagation of vaso occlusive crises which can be analysed by determining the expression of neutrophil antigens such as CD16, CD32, and CD62L. The common FcγR polymorphisms (FcγRIIA and FcγRIIIB) are considered to influence clinical presentation. This study focuses on distribution of FcγR polymorphisms and their association with neutrophil activity among the patients from western India. Methods. In this paper 127 sickle cell anemia patients and 58 patients with sickle-β-thalassemia (median age 12±8.58 years) with variable clinical phenotypes along with 175 normals were investigated. FcγRs polymorphisms were analysed by RFLP and AS-PCR. Activation of neutrophils was measured by flow cytometry. Results. The genotypic frequency of the H/R genotype of FcγRIIA and the NA1/NA1 genotype of FcγRIIIB was significantly decreased in patients compared to normals (P-0.0074, P-0.0471, resp.). We found a significant difference in the expression of CD32 and CD62L among the patients as against normals. A significantly higher expression of CD32 was seen in the milder patients with the H/H genotype (P-0.0231), whereas the expression of CD16 was higher in severe patients with the NA2/NA2 genotype (P-0.0312). Conclusion. The two FcγR polymorphisms had significant association with variable phenotypes of sickle cell disease. The expression of CD62L decreased in our patients indicating activation of neutrophils