Older people are particularly susceptible to infectious and neoplastic diseases of the lung and it is unclear how lifelong exposure to environmental pollutants affects respiratory immune function. In an analysis of human lymph nodes (LNs) from 84 organ donors aged 11–93 years, we found a specific age-related decline in lung-associated, but not gut-associated, LN immune function linked to the accumulation of inhaled atmospheric particulate matter. Increasing densities of particulates were found in lung-associated LNs with age, but not in the corresponding gut-associated LNs. Particulates were specifically contained within CD68⁺CD169⁻ macrophages, which exhibited decreased activation, phagocytic capacity, and altered cytokine production compared with non-particulate-containing macrophages. The structures of B cell follicles and lymphatic drainage were also disrupted in lung-associated LNs with particulates. Our results reveal that the cumulative effects of environmental exposure and age may compromise immune surveillance of the lung via direct effects on immune cell function and lymphoid architecture.

老年人特别容易患肺部传染病和肿瘤性疾病，目前尚不清楚终生接触环境污染物如何影响呼吸系统免疫功能。在对 84 名年龄在 11-93 岁的器官捐献者的人体淋巴结 (LN) 进行的分析中，我们发现肺部相关而非肠道相关的淋巴结免疫功能与吸入大气颗粒物的积累有关，与年龄相关的特定下降事情。随着年龄的增长，在肺相关 LN 中发现颗粒密度增加，但在相应的肠道相关 LN 中没有发现。颗粒物特别包含在 CD68 ⁺ CD169 ^-与不含颗粒的巨噬细胞相比，巨噬细胞表现出活性降低、吞噬能力降低和细胞因子产生改变。B 细胞滤泡的结构和淋巴引流在肺相关 LNs 中也被颗粒物破坏。我们的结果表明，环境暴露和年龄的累积影响可能会通过对免疫细胞功能和淋巴结构的直接影响来损害肺部的免疫监视。