Ischemic stroke alters immune cell niche and chemokine profile in mice independent of spontaneous bacterial infection

摘要: Introduction Stroke-associated pneumonia (SAP) is a major cause of mortality in patients who have suffered from severe ischemic stroke. Although multifactorial nature, stroke-induced immunosuppression plays key role the development SAP. Previous studies using murine model transient middle cerebral artery occlusion (tMCAO) shown that focal stroke induction results functional defects lymphocytes spleen, thymus, and peripheral blood, leading to spontaneous bacterial infection lungs without inoculation. However, how alters immune cell niche expression cytokines chemokines has not been fully characterized. Methods Ischemic was induced mice by tMCAO. Immune profiles brain at 24- 72-hour time points were compared flow cytometric analysis. Cytokine chemokine determined multiplex bead arrays. Tissue damage burden following tMCAO evaluated. Results increases percentage alveolar macrophages, neutrophils, CD11b+ dendritic cells, but reduces CD4+ T CD8+ B natural killer eosinophils lungs. The alteration coincides with significant reduction levels multiple lungs, including CCL3, CCL4, CCL5, CCL17, CCL20, CCL22, CXCL5, CXCL9, CXCL10. Spontaneous tissue tMCAO, however, observed. Conclusion This first report demonstrate proinflammatory mice. These findings suggest directly impacts pulmonary immunity.