RESUMO
Inflammation is a distinguished clinical manifestation of COVID-19 and type 2 diabetes mellitus (T2DM), often associated with inflammatory dysfunctions, insulin resistance, metabolic dysregulation, and other complications. The present study aims to test the hypothesis that serum concentrations of PAR-1 levels differ between COVID-19 diabetic patients (T2DM) and non-diabetic COVID-19 patients and determine their association with different biochemical parameters and inflammatory biomarkers. T2DM patients with COVID-19 (n = 50) with glycated hemoglobin (HbA1c) levels of (9.23 ± 1.66) and non-diabetic COVID-19 patients (n = 50) with HbA1c levels (4.39 ± 0.57) were recruited in this study. The serum PAR-1 levels (ELISA method) were determined in both groups and correlated with parameters such as age, BMI, inflammatory markers including CRP, interleukin 6 (IL-6), tumor necrosis factor-alpha (TNF-α), D-dimer, homocysteine, and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Demographic variables such as BMI (29.21 ± 3.52 vs. controls 21.30 ± 2.11) and HbA1c (9.23 ± 1.66 vs. controls 4.39 ± 0.57) were found to be statistically elevated in COVID-19 T2DM patients compared to non-diabetic COVID-19 patients. The concentrations of several inflammatory biomarkers and PAR-1 were remarkably increased in the COVID-19 T2DM group when compared with the non-diabetic COVID-19 group. The univariate analysis revealed that increased serum PAR-1 estimations were positively correlated with enhanced HbA1c, BMI, inflammatory cytokines, D-dimer, homocysteine, and NT-proBNP. The findings in the current study suggest that increased levels of serum PAR-1 in the bloodstream could potentially serve as an independent biomarker of inflammation in COVID-19 patients with T2DM.
RESUMO
Leukocyte migration from the vascular compartment is critical fornormal lymphocyte recirculation in specific tissues and immune response in inflammatory locations. Leukocyte recruitment, migration to inflammatory areas, and targeting in the extravascular space are caused by cellular stimulation and local expression of adhesion molecules. Intercellular adhesion molecule 1 (ICAM-1) and Vascular cell adhesion molecule 1 (VCAM-1) belong to the immunoglobulin superfamily of cell adhesion molecules (CAM) with a crucial role in mediating the strong adherence of leukocytes to endothelial cells in numerous acute as well as chronic diseases. ICAM-1 and VCAM-1 mediate inflammation and promote leukocyte migration during inflammation. ICAM-1 and VCAM-1 have a large role in regulating homeostasis and in pathologic states such as cancer, atherosclerosis, atrial fibrillation, myocardial infarction, stroke, asthma, obesity, kidney diseases, and much more. In inflammatory conditions and infectious disorders, leukocytes move and cling to the endothelium via multiple intracellular adhesive interactions. It is suggested that combining membrane-bound and soluble ICAM-1 and VCAM-1 into a single unit functional system will further our understanding of their immunoregulatory role as well as their pathophysiological effects on disease. This review focuses on the pathophysiological roles of ICAM-1 and VCAM-1 in various inflammatory and other diseases as well as their emerging cardiovascular role during the COVID-19 pandemic.