Impact of Ambient Particulate Matter on the Skin’s Immune System

Abstract

Skin is the outermost layer of the human body. The main functions of the skin include protecting the body from external harm, maintaining homeostasis, sensory perception, and thermoregulation. The skin contains many immune cells that participate both in innate and adaptive immunity. Proper skin function is disrupted when exposed to harmful environmental pollutants, such as airborne particulate matter, which aggravates the severity of skin diseases, such as eczema, psoriasis, and atopic dermatitis. Air pollution kills approximately five million individuals annually, and the death rate continues to rise. Many studies have been conducted regarding the role of particulate matter in the respiratory system. In contrast, there is minimal data available on the impact of particulate matter on the skin’s immune system. However, there is more information available in recent years; for instance, PM exposure impairs skin barrier function by activating different inflammatory pathways, dysregulates T cell differentiation, activates NLRP3 inflammasome, and induces pro-inflammatory cytokine secretion. Therefore, this review assiduously discusses the impact of ambient particulate matter on the skin’s immune system. effector homeostasis TLRs triggers signaling via MyD88 and downstream molecules, which leads to nuclear translocation of NF-κB, where it binds to the promoter region of interleukins, including IL-6. In addition, NLRP3 inflammasome is also activated on PM exposure. Consequently, there is increase in pro-inflammatory cytokines secretion, including IL-1β, which leads to skin inflammation. AhR, aryl hydrocarbon receptor; AP-1, activator protein 1; DC, dendritic cell; IFN, interferon; IL, interleukin; LC, Langerhans cell; MyD88, myeloid differentiation primary response 88; NF-κB, nuclear factor-κB; NLRP3, NOD-, LRR- and pyrin domain-containing protein 3; PAH, polycyclic aromatic hydrocarbon; PM, particulate matter; TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin; Th, T helper cell type; TLR, toll-like receptor; Treg, regulatory T cell. cascades, unbalancing T cell differentiation, triggering NLRP3 inflammasome activation, and inducing pro-inflammatory cytokine production. However, future research should focus on mechanistic investigations by using cell-based and animal models to understand how PM adversely affects skin’s immune system. This endeavour will demand for solving human health issues by PM exposure. Overall, this review will broaden our knowledge and help develop better strategies to manage human health challenges associated with PM.