The Role of Pulmonary and Systemic Immunosenescence in Acute Lung Injury.

摘要: Acute lung injury (ALI) is associated with increased morbidity and mortality in the elderly (> 65 years), but knowledge about origin effects of immunosenescence ALI limited. Here, we investigated immune response at pulmonary, systemic cellular level young (2-3 months) old (18-19 C57BL/6J mice to localize characterize ALI. was induced by intranasal lipopolysaccharide (LPS) application animals were sacrificed 24 or 72 h later. Pulmonary inflammation analyzing histopathology, bronchoalveolar lavage fluid (BALF) cytometry cytokine expression. Systemic serum expression, spleen lymphocyte populations gut microbiome analyzed, as well activation alveolar bone marrow derived macrophages (BMDM) vitro. pathology more severe compared mice. Old showed significantly inflammatory cells pro-inflammatory cyto- chemokines (TNFα, IL-6, MCP-1, CXCL1, MIP-1α) BALF, a delayed expression cytokines adaptive immunity microbial elimination (IL-12 IFNγ). Alveolar macrophages, not BMDM, greater after vivo vitro stimulation LPS. No enhanced detected LPS exposure, IL-12 IFNγ. Furthermore, had less CD8+ T-cells NK regulatory distinct structure. The results our study show an macrophage signaling lungs, systemically, suggesting key role senescent A decrease stimulators advancing age might further promote susceptibility worse prognosis elderly.