Exosomal programmed death-ligand 1 is associated with post-intracerebral hemorrhage pneumonia.

BACKGROUND

Post-stroke immunosuppression elevates the risk of stroke-associated pneumonia (SAP). Our earlier research indicated that perihematomal neuron-derived PD-L1 may play a role in peripheral immunosuppression following intracerebral hemorrhage (ICH); however, the specific carriers of PD-L1 and its potential as a predictor for SAP risk are yet to be determined.

MATERIALS AND

METHODS

We hypothesize that elevated levels of exosomal PD-L1 in peripheral blood after ICH mediate immune suppression and increase the risk of SAP. This observational study aimed to investigate the levels of exosomal PD-L1 post-ICH and their relationship with SAP. In an exploratory cohort of 39 patients with ICH and 24 healthy controls and a validation cohort of 144 patients with ICH.

RESULTS

At admission, patients with ICH exhibited significantly increased exosome numbers in their peripheral blood, with these exosomes showing high expression of the neuronal marker neural cell adhesion molecule L1, suggesting a brain origin. Exosomal PD-L1 levels were elevated in patients with ICH compared to healthy controls and were higher in patients with SAP than those without. After adjusting for confounders, exosomal PD-L1 was confirmed to be independently associated with SAP in both the exploratory cohort and validation cohort.

CONCLUSIONS

Brain-derived exosomes with high expression of PD-L1 are substantially released into the periphery after ICH. Elevated exosomal PD-L1 levels correlate with an increased risk of SAP.