Overproduction of CXC chemokines CXCL1, CXCL9, CXCL10 and CXCL12 in β-thalassemia major or patients

Abstract

BACKGROUND AND OBJECTIVESβ-thalassemia major is one of the most frequent hematological genetic disorders, worldwide. Chemokines are the main components of the immune system and play fundamental roles in pathogenesis of inflammatory disorders. Therefore, the present study aimed to examine whether serum CXC chemokines are altered in β-thalassemia major patients.DESIGN AND SETTINGSWe enrolled 63 β-thalassemia patients and 80 controls in this cross-sectional study, which was performed during 2012–2013 in Kerman, Iran.METHODSWe enrolled 63 β-thalassemia patients and 80 controls in the present study. Patients were selected from referrals to Samenolhojaj clinic for thalassemia, Kerman, Iran. The circulating levels of CXCL1, CXCL9, CXCL10, and CXCL12 were detected by enzyme-linked immunosorbent assay in thalassemia patients and healthy controls immediately after blood collection. Data were analyzed by χ2, t-test, and analysis of variance statistical methods and using SPSS, version 13 (SPSS Inc., Chicago, IL).RESULTSThe results of the study demonstrated a significant elevation of CXCL1, CXCL9, CXCL10, and CXCL12 in thalassemia patients than in control. These results also demonstrated that serum chemokine levels are related to transfusion duration and post-transfusion viral infections.CONCLUSIONAccording to the results obtained, it can probably be concluded that chemokines are also involved in the pathogenesis of β-thalassemia major and its clinical complications in addition to several other parameters.

Serum concentration of angiogenic (CXCL1, CXCL12) and angiostasis (CXCL9, CXCL10) CXC chemokines are differentially altered in normal and gestational diabetes mellitus associated pregnancies

“…CXCL1, CXCL9 and CXCL10 all fit in pro-inflammatory and inducible, whilst, CXCL12 is functionally a constitutive and homeostatic chemokine [16][17][18]. CXCL1 and CXCL12 both exhibit angiogenesis, activities whereas, CXCL9 and CXCL10 have antiangiogenesis properties and display angiostasis activities [19][20][21]. CXCL9 and CXCL10 exert their functions via binding to CXCR3 (a specific receptor for CXCL9 and CXCL10) [22,23].…”

Acute Promyelocytic Leukemia in a Woman with Thalassemia Intermedia: Case Report and Review of Literature on Hematological Malignancies in β-Thalassemia Patients

“…Likewise, treatment with ATRA promotes a striking up-regulation of adhesion molecules on APL blast cells such as CD11b, CD11c, CD15, CD65, and CD54, thus leading to lung infiltration and inflammation [ 41 , 42 , 43 ]. Finally, there is a significant elevation of chemokine levels (CXCL1, CXCL9, CXCL10, and CXCL12) in TD β-thalassemia patients [ 44 ], while ATRA differentiation therapy can itself induce chemokine production in the lungs and chemokine receptors expression in APL cells, triggering migration of leukemic cells [ 45 ].…”