Abstract
ObjectiveExposure to air particulate matter (PM) is associated with chronic inflammatory and autoimmune diseases. Macrophages are responsible for the regulation of chronic inflammation. However, whether PM affects macrophage polarization remains unclear. The aim of this study was to evaluate whether nontoxic concentrations of urban PM are able to prime macrophages to altered inflammatory response upon LPS challenge.MethodsWe used two forms of the urban particulate matter SRM 1648a, intact PM and PM deprived of organic compounds (PM∆C). Peritoneal murine macrophages were exposed to different concentrations of PM for 24 h and then challenged with LPS. Production of inflammatory mediators by macrophages was measured to test immunostimulatory/priming capacity of PM.ResultsParticulate matter used at non-cytotoxic concentrations induced a dose-dependent production of proinflammatory cytokines (TNF-α, IL-6, IL-12p40). By contrast, PM∆C were not able to stimulate macrophages. However, macrophages primed with both forms of PM show proinflammatory response upon LPS challenge.ConclusionsOur data indicate that exposure of macrophages to low concentrations of PM may prime the cells to hyperinflammatory response upon contact with LPS. Further studies are necessary to explain whether the exposure of patients suffering from chronic inflammatory diseases to particulate matter is responsible for the exacerbation of clinical symptoms during bacterial infections.
Highlights
The last decade has significantly changed the perception of etiopathogenesis of inflammatory and autoimmune disorders (AIDs) such as asthma, chronic obstructive pulmonary disease, rheumatoid arthritis and atherosclerosis [1, 2]
Exposure to the air particulate matter is epidemiologically associated with various chronic inflammatory and autoimmune diseases
Increased incidence and exacerbation of cardiopulmonary disorders has been found to associated with elevated levels of urban particulate matter [6, 25, 26]
Summary
The last decade has significantly changed the perception of etiopathogenesis of inflammatory and autoimmune disorders (AIDs) such as asthma, chronic obstructive pulmonary disease, rheumatoid arthritis and atherosclerosis [1, 2]. Development of these chronic civilization diseases is triggered by a set of factors, both genetic and environmental [4]. Among environmental factors, such as exposure to tobacco smoke, infectious agents, radiation and ultraviolet light exposure, air pollution seems to be involved in the pathogenesis of AIDs [5]. The increased concentration of pollutants in the air has been strongly associated with lung inflammatory diseases [6]
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