Air particulate matter SRM 1648a primes macrophages to hyperinflammatory response after LPS stimulation

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.

Transition Metal Containing Particulate Matter Promotes Th1 and Th17 Inflammatory Response by Monocyte Activation in Organic and Inorganic Compounds Dependent Manner

“…Effect of TMCPM on the activity of human CD4+ T cell subsets was investigated after five hours of healthy donor PBMCs exposure to NIST or LAP particles. The concentrations of NIST and LAP used in the study were established experimentally in a range from 1-100 μg/mL, as used at higher concentrations were cytotoxic (data not shown), confirming previous reports [22]. At first, we checked weather TMCPM may affect the proportion of CD4+ T cells and the expression of CD4 on their surface, as was documented for PMA and ionomycin [25][26][27], potent activators of T cells.…”

“…In keeping, recently Mikrut et al, using the same preparations of TMCPM showed that the organic fraction from NIST was mostly responsible for singlet oxygen photogeneration when compared with LAP particles [23]. In another study, Gawda et al showed that the urban particulate matter SRM 1648a induced in vitro a dose-dependent production of pro-inflammatory cytokines (TNF-α, IL-6, IL-12p40) by murine macrophages [22]. Interestingly, under the same conditions, LAP particles were not able to stimulate macrophages, however the cells primed with NIST or LAP showed a strong pro-inflammatory response upon LPS challenge.…”

“…Two different preparations of TMCPM (transition metal containing particulate matter) were used in the study: SRM 1648a-standard urban particulate matter (purchased from the National Institute for Standards and Technology, Gaithersburg, MD, USA), designated as NIST, which is a conglomeration of fine and ultrafine particles (mean particle diameter 5.85 µm), containing ca. 13% of carbon, including 10.5% of organic carbon [22] and LAP-SRM 1648a particulate matter treated within 120 min with cold oxygen plasma for the removal of organic compounds from the reference material. Samples of LAP, with removed organic content (containing less than 2% of organic carbon, and less than 1% of nitrogen) were prepared in the Department of Inorganic Chemistry, Jagiellonian University, Krakow, Poland, as described previously [23].…”

Particulate matter exposure aggravates osteoarthritis severity

“…Similar results were found for cytokine expression in the lung. Several pro-inflammatory factors are released from macrophages, such as ILs and TNF-α [13,47]. Previous article suggested that different sizes of particles may through different regulated pathways to affect the alveolar macrophages, such as coarse particles are via endotoxin-toll-like receptor (TLR) 4 pathway; while the fine and ultrafine particles are transition metals and/or polyaromatic hydrocarbons to generate ROS to activate innate immune responses [13].…”

Urban air PM modifies differently immune defense responses against bacterial and viral infections in vitro

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