The Inflammatory Preatherosclerotic Remodeling Induced by Intermittent Hypoxia Is Attenuated by RANTES/CCL5 Inhibition.
Arnaud, Claire 1,2; Beguin, Pauline C. 1,2; Lantuejoul, Sylvie 2,4,7; Pepin, Jean-Louis 1,2,3; Guillermet, Christiane 4; Pelli, Graziano 8; Burger, Fabienne 8; Buatois, Vanessa 9; Ribuot, Christophe 1,2; Baguet, Jean-Philippe 2,5,10; Mach, Francois 8; Levy, Patrick 1,2,3,*; Dematteis, Maurice 1,2,6,*
[Article] American Journal of Respiratory & Critical Care Medicine. 184(6):724-731, September 15, 2011.

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Rationale: The highly prevalent obstructive sleep apnea syndrome (OSA) with its main component intermittent hypoxia (IH) is a risk factor for cardiovascular mortality. The poor knowledge of its pathophysiology has limited the development of specific treatments, whereas the gold standard treatment, continuous positive airway pressure, may not fully reverse the chronic consequences of OSA and has limited acceptance in some patients.

Objectives: To examine the contribution of IH-induced inflammation to the cardiovascular complications of OSA.

Methods: We investigated systemic and vascular inflammatory changes in C57BL6 mice exposed to IH (21-5% Symbol, 60-s cycle) or normoxia 8 hours per day up to 14 days. Vascular alterations were reassessed in mice treated with a blocking antibody of regulated upon activation, normal T-cell expressed and secreted (RANTES)/CC chemokine ligand 5 (CCL5) signaling pathway, or with the IgG isotype control throughout the IH exposure.

(C) 2011 American Thoracic Society