The accumulation of inhaled particulate matter can impair the immune function and structure of the lymph nodes in the human lungs

Older adults are particularly susceptible to pulmonary infectious and neoplastic diseases, 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 age-specific age-related declines in lung-associated (rather than gut-related
) LN immune function associated with the accumulation of inhaled atmospheric particulate matter.
With age, an increase in particle density is found in lung-associated LNs, but not
in the corresponding gut-associated LNs.
CD68⁺CD169⁺ macrophages specifically contain microparticles compared with macrophages without particles, exhibiting decreased activity, decreased phagocytic capacity, and altered
cytokine production.
The particles also disrupt the B-cell follicular structure and lymphatic drainage
of lung-associated LNs.
Our findings suggest that the cumulative effects of environmental exposure and age may disrupt immune monitoring
of the lungs by directly affecting immune cell function and lymphocyte structure.

The demographics of the world's population are changing rapidly, with it predicted that by 2050, people aged 65 or over will make up more than
20 per cent of the population.
Since most health care costs, morbidity and mortality are borne by people over the age of 55, there is a need to better understand the mechanisms by
which ageing increases susceptibility to disease.
In particular, with age, there is a significant and alarming increase in the incidence and severity of lung and respiratory diseases
.
Older adults are at increased risk of lung injury and at increased risk of serious consequences from respiratory viruses such as influenza 3 and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with infection deaths in individuals under 75 years of age more than
80 times higher than in younger people.
In addition, lung tumor diseases, including small cell lung cancer, mainly affect people
over the age of 60.

Aging changes in the immune system are associated with
an increased burden of disease in older adults.
With age, immune cells and functional mediators undergo intrinsic changes, leading to a weakened adaptive immune response, increased inflammation, and weakened regulation, thereby undermining anti-pathogen and anti-tumor immunity
.
However, the mechanism by which respiratory immunity is biased and decreased with age is unclear
.
In addition, aging and its effects on the respiratory tract are formed by long-term exposure to the environment through inhalation, although the role environmental damage plays in age-related damage to the immune system is unclear
.

Human immunosenescence studies sample blood is the most readily available site
.
However, the immune response occurs at the mucosa and barrier site of infection and associated lymphoid organs
.
As shown in mouse models, for respiratory infection responses, lung-associated lymph nodes (LLNs) are essential
for adaptive immune responses to new and recurrent pathogens.
Antigens encountered in the lungs enter LLNs via lymph, where an adaptive immune response is initiated, including T cell activation and interaction with B cells in specialized lymphatic follicles to promote humoral immunity
.
Age-related LNs effects have been found in mice, and morphological changes with age have also been reported in human LNs; However, analysis of human LNs aging and its effects on immune response and function has not been conducted
.
As part of their immune surveillance role, LNs also filter impurities in tissues through lymphoid tissue, although the effects of this broader role of LNs on the human immune response remain unexplored
.
In this study, we used anatomical methods to study the cells, structure, and functional niches of tissue draining lymph nodes in samples from human organ donors of different ages, revealing local, age-related changes in LLNs due to accumulation of atmospheric particulate matter inhaled by environmental pollutants
.