The Serum Level of CXCL9, CXCL10, and CXCL11 and the Expression of CXCR3 of Peripheral Blood Mononuclear Cells in Brucellosis Patients.

Brucella spp. can replicate in human endothelial cells, inducing an inflammatory response with increased expression of chemokines. Although Brucella infects humans, its ability to induce the production of chemokines by lung cells is unknown. Therefore, the current investigation was designed to examine the association between brucellosis and CXCL9, 10, and 11 chemokines. The patient group included 71 patients suffering from Brucella infection and the control group consisted of 50 healthy ranchers from the same geographical area. Serum levels of CXCL9, CXCL10, and CXCL11 were analyzed by ELISA. The fold changes of CXCR3 expression against ß-actin were determined by real-time-PCR technique. Western blotting analysis was also applied for evaluating the expression of CXCR3 at protein level. The results of this study showed that the serum levels of CXCL9, CXCL10, and CXCL11 are significantly increased in acute brucellosis patients in comparison to control as indicated by ELISA test, mRNA levels of CXCR3 by Real-time PCR as well as protein levels of CXCR3 by Western blot analysis. According to findings, these chemokines have the potential to serve as markers for brucellosis patients. Taken together, cytokine/chemokine network was active in acute brucellosis patients, and it is suggested to evaluate other cytokines in future studies.

The Involvement of CXC Motif Chemokine Ligand 10 (CXCL10) and Its Related Chemokines in the Pathogenesis of Coronary Artery Disease and in the COVID-19 Vaccination: A Narrative Review.

Coronary artery disease (CAD) and coronary heart disease (CHD) constitute two of the leading causes of death in Europe, USA and the rest of the world. According to the latest reports of the Iranian National Health Ministry, CAD is the main cause of death in Iranian patients with an age over 35 years despite a significant reduction in mortality due to early interventional treatments in the context of an acute coronary syndrome (ACS). Inflammation plays a fundamental role in coronary atherogenesis, atherosclerotic plaque formation, acute coronary thrombosis and CAD establishment. Chemokines are well-recognized mediators of inflammation involved in several bio-functions such as leucocyte migration in response to inflammatory signals and oxidative vascular injury. Different chemokines serve as chemo-attractants for a wide variety of cell types including immune cells. CXC motif chemokine ligand 10 (CXCL10), also known as interferon gamma-induced protein 10 (IP-10/CXLC10), is a chemokine with inflammatory features whereas CXC chemokine receptor 3 (CXCR3) serves as a shared receptor for CXCL9, 10 and 11. These chemokines mediate immune responses through the activation and recruitment of leukocytes, eosinophils, monocytes and natural killer (NK) cells. CXCL10, interleukin (IL-15) and interferon (IFN-g) are increased after a COVID-19 vaccination with a BNT162b2 mRNA (Pfizer/BioNTech) vaccine and are enriched by tumor necrosis factor alpha (TNF-α) and IL-6 after the second vaccination. The aim of the present study is the presentation of the elucidation of the crucial role of CXCL10 in the patho-physiology and pathogenesis of CAD and in identifying markers associated with the vaccination resulting in antibody development.