In a recent research briefing published in Natural medicineresearchers have emphasized the importance of air quality in maintaining immune health throughout human life, particularly lung-related immunity, due to the lungs’ constant exposure to the environment.
Background
Aging worsens susceptibility to disease, a harsh reality that has emerged during the unprecedented coronavirus disease 2019 (COVID-19) pandemic. However, older individuals are not only more susceptible to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, but are also prone to other lung diseases, such as chronic obstructive pulmonary disease (COPD) and lung cancer.
As people age, age-related changes in immune cells and subsequent systemic inflammation functionally impair their acquired immunity, likely increasing their susceptibility to disease. Since the immune system resides in mucosal and lymphoid tissues, the effect of increasing age on local immune responses in these areas needs to be evaluated in detail.
A better understanding of the physiological mechanisms that exacerbate disease susceptibility in the elderly could help reduce health care costs associated with disease in a rapidly aging world population. It is noteworthy that individuals in the age group of 60 years and older consume a large proportion of health care resources worldwide.
About studying
In this study, researchers obtained lymph node (LN) samples from human organ donors of different age groups to investigate the effect of particles on their immune cells. Because they observed distinct effects of air pollutants on lung LN compared to gut LN, they used quantitative imaging to visualize LN architecture across all LN sites. They further used functional and cellular assays to analyze the effect of aging on LN.
Study results
The researchers noted an accumulation of black particles in lung LNs that increased substantially in samples from individuals older than 40 years. In contrast, LNs related to the intestine remained beige in color and had no black particles.
Particles in lung-associated LNs remained confined to a specific population of macrophages nested in the T cell expanse (not in follicles). These macrophage subsets showed functional changes such as impaired cytokine secretion, reduced activation, and markedly reduced phagocytic potential. Interestingly, macrophages without particles deposited inside the same LN showed no functional changes. Finally, the researchers also found that particle accumulation in lung LNs led to age-related changes in the structural integrity of LNs due to impairments in lymphatic drainage and B cell follicles.
Together, the study results demonstrated the direct and harmful effects of inhaled particles on acquired and innate immune processes that build up over time in the lymphoid system responsible for immune surveillance of the respiratory system, particularly the lungs.
When lung-associated LNs become clogged with particles, their ability to filter toxins, dangerous antigens, and microbial pathogens is substantially reduced. The results worsen with age, which to some extent rationalizes the increased risk of respiratory diseases in the elderly compared to the younger population.
Conclusions
The current study offered new insights into how environmental pollutants interact and alter the human immune system by examining LN samples rather than blood samples from deceased organ donors of different age groups.
Future studies should investigate the mechanisms that specific macrophages in lung LNs use to internalize particles. Studies should also investigate whether these macrophages are LN residents, derivatives of lung macrophages, or migrate to the lung from other LN sites (eg, mucosal sites). More research is also needed to examine the effects of particle accumulation on pathways other than the phagocytosis pathway in LNs that destroy cellular debris and microbial pathogens.
In addition, the study should motivate further research investigating the effects of carbon emissions and other types of pollution on the human immune system.
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