LONGECITY

Extracellular adenosine signaling reverses the age‐driven decline in the ability of neutrophils to kill Streptococcus pneumoniae

https://onlinelibrar...1111/acel.13218

 

Extracellular adenosine is known to regulate PMN function (Barletta et al., 2012), and more recently, the role of this pathway in host resistance against pulmonary infections has been also highlighted (Lee & Yilmaz, 2018)...

 

.. we demonstrate here for the first time that immunosenescence of PMNs is shaped by the EAD (Exracellular Adenosine) pathway. We find that the age‐driven impairment in bacterial killing by these innate immune cells is largely due to a decrease in EAD production and signaling. Importantly, supplementing with EAD and triggering A1 receptor signaling fully reverses the age‐driven decline in PMN antimicrobial function.

 

This has serious implications for considering the future use of clinically available adenosine‐based drugs (Jacobson, Tosh, Jain, & Gao, 2019) to combat immunosenescence and pneumococcal pneumonia in the susceptible elderly population.

 

So neutrophils (and perhaps other immune cells) have reduced function when there is less EAD (Extracellular Adenosine), but their function is restored when the EAD level can be increased,

Although the discussion is around antimicrobial effects, this seems like it could have implications for COVID-19 too, at least in terms of helping with secondary pneumonia if not the disease itself.

So what raises adenosine levels in the body in general, or in the lungs?