Brain circulation · 2025
Exosomal programmed death-ligand 1 is associated with post-intracerebral hemorrhage pneumonia.
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Gao Bin, Zhang Ying, Cheng Nuo, Ge Shunnan, Lu Zhichao, Wang Hong, He Wenyan, Shi Wei, Qu Yan, Zhao Xingquan, Shi Fu-Dong, Shi Kaibin
Аннотация
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.
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.