An update on immunologic mechanisms in the respiratory mucosa in response to air pollutants

Abstract

Every day, we breathe in more than 10,000 L of air that contains a variety of air pollutants that can pose negative consequences to lung health. The respiratory mucosa formed by the airway epithelium is the first point of contact for air pollution in the lung, functioning as a mechanical and immunologic barrier. Under normal circumstances, airway epithelial cells connected by tight junctions secrete mucus, airway surface lining fluid, host defense peptides, and antioxidants and express innate immune pattern recognition receptors to respond to inhaled foreign substances and pathogens. Under conditions of air pollution exposure, the defenses of the airway epithelium are compromised by reductions in barrier function, impaired host defense to pathogens, and exaggerated inflammatory responses. Central to the mechanical and immunologic changes induced by air pollution are activation of redox-sensitive pathways and a role for antioxidants in normalizing these negative effects. Genetic variants in genes important in epithelial cell function and phenotype contribute to a diversity of responses to air pollution in the population at the individual and group levels and suggest a need for personalized approaches to attenuate the respiratory mucosal immune responses to air pollution.

Transcriptomic and barrier responses of human airway epithelial cells exposed to cannabis smoke

“…To complement the mechanical barrier of the lung, the airway epithelium is able to produce and host-defence peptides and antiviral mediators to protect from pathogens (Parker and Prince, 2011;Huff et al, 2019). Tobacco smoke has been reported to compromise the ability of airway epithelial cells to effectively control both bacterial and viral insults (Hudy et al, 2010;Eddleston et al, 2011;Rider et al, 2011;Amatngalim et al, 2016).…”

Spatio-temporal co-occurrence of hotspots of tuberculosis, poverty and air pollution in Lima, Peru

“…Previous studies in Peru have explored the effect of air pollution as a determinant of asthma [27]. The most important effects of air pollution manifest in the upper respiratory tract where it alters immune response [8], contributing as a susceptibility factor for various respiratory diseases [28]. One study showed impaired the expression of CD69, IFN-γ and TNF-α when human peripheral blood mononuclear cells are exposed to Mycobacterium tuberculosis [29].…”

“…Environmental factors such as pollution and suspended particles are considered to play important roles in the development of TB [7]. This is explained by secretion clearance impairment by epithelial cells of the respiratory tract which is the primary defense mechanism against Mycobacterium tuberculosis [8].…”

Expression of the endocannabinoid system in the human airway epithelial cells – Impact of sex and chronic respiratory disease status

“…Airway epithelial cells carry out a number of functions such as providing a physical barrier against microbial infiltration, maintaining the inflammatory microenvironment, and releasing immune mediators to recruit leukocytes to the site of insult. It has been demonstrated that the inhalation of air pollution, tobacco smoke, and cannabis smoke can compromise airway epithelial function(30-32). Notably, recent findings show that cannabis smoke exposure can lead to impaired airway epithelium barrier integrity, attenuated antiviral capacity, and exacerbated inflammatory response to immune challenges(31, 32).…”