Adenosine Signaling via the A1 Receptor Reverses Age-Related Decline in Neutrophil Function

The objective of this study was to explore the age-driven changes in the EAD pathway and its impact on PMN function. PMNs from old mice failed to efficiently kill pneumococci ex vivo; however, supplementation with adenosine rescued this defect. To identify which adenosine receptors is involved, we used specific agonists and inhibitors. We found that A1 receptor signaling was crucial for PMN function as inhibition or genetic ablation of A1 impaired the ability of PMNs from young mice to kill pneumococci. Importantly, activation of A1 receptors rescued the age-associated defect in PMN function. In exploring mechanisms, we found that PMNs from old mice failed to efficiently kill engulfed pneumococci and that A1 receptor controlled intracellular killing. In summary, targeting the EAD pathway reverses the age-driven decline in PMN antimicrobial function, which has serious implications in combating infections. Link: https://doi.org/10.1111/acel.13218
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs