Induction of the Chemokines CCL3α, CCL3α and CCL5 in Atherosclerotic Patients
Alyaa Mousa, Amani Al-Zaki, Safa Taha and Moiz Bakhiet
DOI : 10.3844/ajisp.2007.45.51
American Journal of Immunology
Volume 3, Issue 2
Chemokines recruit immune cells to inflammatory sites and promote the process of inflammation. The role of these mediators in the disease process in atherosclerosis is not fully studied. The spontaneous mRNA expression and intracellular protein production of the potential inflammatory chemokines CCL3Î± and CCL3Î² (macrophage- inflammatory protein-1Î± and Î²; CCR3Î±/Î² ligand) and CCL5 (regulated upon activation, normal T cell expressed and secreted (RANTES; CCR5 ligand) in atherosclerotic patients was examined together with the effects of the chlamydial antigen HSP60 and LPS on the gene expression and protein induction of these mediators. Detection of chemokine mRNA and protein levels was assessed by in situ hybridization and immunohistochemistry respectively. The examined chemokines were detected at significantly high levels on atherosclerotic patients compared to healthy controls at both mRNA and protein levels. Stimulation with HSP60 and LPS from Chlamydia pneumoniae (C. pneumoniae) and E. coli showed increased numbers of CCL3Î±, CCL3Î² and CCL5 mRNA expressing cells in patients compared to health controls. Protein translation of these chemokines was depicted in correspondence to the mRNA gene expression for all examined chemokines spontaneously and after stimulation with chlamydial HSP60 and LPS and E. coli LPS. Thus, the herein data demonstrate the induction of potential inflammatory chemokines in atherosclerotic patients and that bacterial antigens play a role in the immunopathologic events in this disease by generating more inflammatory mediators.
© 2007 Alyaa Mousa, Amani Al-Zaki, Safa Taha and Moiz Bakhiet. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.