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Electronic Letters to:
- Neurobiology of Disease:
Barry W. McColl, Nancy J. Rothwell, and Stuart M. Allan- Systemic Inflammatory Stimulus Potentiates the Acute Phase and CXC Chemokine Responses to Experimental Stroke and Exacerbates Brain Damage via Interleukin-1- and Neutrophil-Dependent Mechanisms
J. Neurosci. 2007; 27: 4403-4412[Abstract] [Full text] [PDF]
eLetters: Submit a response to this article
Electronic letters published:
The Role of CXCL5 in Experimental Stroke
- Issam Zineh (31 October 2007)
The Role of CXCL5 in Experimental Stroke 31 October 2007 
Issam Zineh,
Assistant Professor
University of Florida College of Pharmacy, PO Box 100486, Gainesville, FL, USA 32610Send letter to journal:
Re: The Role of CXCL5 in Experimental Stroke
zineh{at}cop.ufl.edu Issam Zineh
McColl and colleagues present compelling data that systemic inflammation exacerbates central brain injury in experimental stroke. They offer mechanistic insights into this process and implicate IL-1-mediated upregulation of the neutrophilic chemokines CXCL1/KC and CXCL2/MIP-2a as a critical determinant of cerebral ischemic injury. We suggest a potential role for CXCL5 in mediating these detrimental effects. CXCL5 belongs to the CXC family of chemokines and is a potent neutrophil attractor and activator. In humans, the protein product of the CXCL5 gene (ENA-78) has an approximately 50% amino acid homology with CXCL1 and CXCL2. In addition, CXCL5 is upregulated by LPS and IL-1, and associates with enhanced neutrophil influx in inflammatory conditions. Zaremba and colleagues (2006) demonstrated two-fold higher CXCL5 concentrations in the cerebrospinal fluid of stroke patients compared with controls within 24 hours, along with a positive correlation between CXCL5 levels and the volume of hypodense areas on brain CT. In addition, we have previously demonstrated that the HMG-CoA reductase inhibitor, atorvastatin, lowers CXCL5 production from human endothelial cells in a dose-dependent fashion (Zineh 2006). Given that statins reduce stroke risk in patients and the known effects of CXCL5 in vivo, it would be interesting to examine the role of CXCL5 in the experimental stroke model outlined by McColl and colleagues.
Zaremba J, Skrobański P, Losy J (2006) The level of chemokine CXCL5 in the cerebrospinal fluid is increased during the first 24 hours of ischaemic stroke and correlates with the size of early brain damage. Folia Morphol (Warsz) 65(1):1-5.
Zineh I, Luo X, Welder GJ, Debella AE, Wessel TR, Arant CB, Schofield RS, Chegini N (2006) Modulatory effects of atorvastatin on endothelial cell-derived chemokines, cytokines, and angiogenic factors. Pharmacotherapy 26(3):333-40.
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