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Like the skin, the lung is another barrier tissue constantly exposed to environmental and microbial pathogens. Individuals aged 75–84 have nearly 20-times higher morbidity and mortality compared to younger adults after acute lung injury [57]. People over age 65 account for 70% of influenza- and pneumonia-related hospitalizations [58], and studies in mice show that aging increases susceptibility to secondary bacterial challenges after influenza infection [59]. Together, these studies highlight multiple defects in the aging lung, including local immune responsiveness and tissue maintenance and repair, which increases host vulnerability to lung damage and disease. Age-related changes in the lung milieu are significant given that even in young animals the lung environment strongly regulates the activation and function of resident immune cells [60]. In a prospective study of emergency room patients with burn inhalation injuries, older patients were at increased risk of death after burn injury and had higher concentrations of inflammatory cytokines in their serum and bronchoalveolar lavage fluid [61]. High vascularization within the lung makes it a unique site that can be rapidly infiltrated by circulating leukocytes. Increased neutrophil infiltration and activation is associated with excess immune pathology during infection in mouse and human studies [25, 62–66]. As described above, dysregulation of neutrophil responses and impaired chemotaxis could impair pathogen clearance and prolong detrimental inflammatory responses in the lungs of elderly individuals.