Involvement of immunosenescence in the frailty syndrome (85.13)

Abstract A determinant factor of immunosenescence is the involution of the T-cell compartment, due to a decline in thymic generation of a diverse T-cell repertoire, as well as in peripheral T-cell homeostasis. Human immunosenescence was investigated through measurement of telomere length by Q-PCR, evaluation of thymic output by Sj and VβTREC methodology, analysis of T-cell phenotype profile, and multiplex cytokine production after polyclonal stimulation. The diseases scrutinized in the elders were pneumonia, heart failure and hip fracture. TREC value was negatively correlated with age, but no significant relationship could be evidenced with pathological states. A significant rise in pro-inflammatory cytokines IL-6, IFNγ and TNFα was observed in elderly vs. young controls, while IL-10 was significantly decreased. The cytokine profiles as analyzed by protein array showed at least three different patterns: either increased in elderly vs. young and decreased in pathologic states, either increasing or showing no modifications in all cases. A significant shortening of telomere length in the elderly was observed when compared to young controls. There was a significant decrease between healthy and sick elders. Significant correlations were evidenced between morbidity and some immune parameters, supporting that immunosenescence contributes to the frailty syndrome. Supported by the Walloon Region - Senegene project