Role of CD8+ T lymphocytes in pathogenesis of pneumonia after acute cerebral infarction

Objective To explore the role of CD8+ T lymphocyte in the pathogenesis of pneumonia after acute cerebral infarction by laboratory testing combined with clinical evaluation. Methods A total of 60 patients with acute cerebral infarction hospitalized at Department of Neurology of East Hospital Affiliated to Tongji University and Jiangyin People′s Hospital Affiliated to Southeast University from December 2014 to December 2016 were enrolled. Venous blood was collected from patients with cerebral infarction in 48 h of onset, and peripheral blood mononuclear cells were isolated. Cellular CD107a, intracellular IFN-γ and TNF-α were detected. According to whether pneumonia occurred during hospitalization, the 60 cases were divided into a pneumonia group or a non-pneumonia group. The difference in the positive expression of CD107a, IFN-γ and TNF-α was compared among the pneumonia group stimulated with hybrid viral peptides, non-pneumonia group stimulated with hybrid viral peptides, pneumonia group without hybrid viral peptide stimulation and non-pneumonia group without hybrid viral peptide stimulation. Results After stimulation with the hybrid viral peptides, CD107a positive expression rates in CD8+ T lymphocytes (10.6±3.7% vs 15.6±4.3%, t=3.192, P=0.004) and intracellular IFN-γ [(15.3±4.3)% vs (20.0±5.1)%, t=4.127, P<0.001] and TNF-α positive expression rates [(15.1±4.4)% vs (19.3±4.7)%, t=3.621, P<0.001] were significantly lower in the pneumonia group than in the non-pneumonia group. Without stimulation with the hybrid viral peptides, intracellular IFN-γ [(3.0±1.2)% vs (3.6±1.7)%, t=3.734, P<0.001] and TNF-α positive expression rates [(3.3±1.4)% vs (4.1±2.1)%, t=3.189, P=0.004] were significantly lower in the pneumonia group than in the non-pneumonia group. Conclusion The inhibition of cytotoxicity of CD8+ T lymphocytes is an important mechanism involved in the pathogenesis of pneumonia after acute cerebral infarction. Key words: Cerebral infarction; Pneumonia; T lymphocytes