The innate and adaptive immune response induced by alveolar macrophages exposed to ambient particulate matter

Balanced TH1 and TH2 immunopotentiating effects of silicates partly containing nanoparticles present in calcined serpentine

“…Similarly, these exposures to CS also induced the secretion of IL-4 and IL-10 cytokines and IgG 1 . Thus, while it was already shown that CS appeared to improve the responsiveness of macrophages, it seemed to also do so with T-(and indirectly, B-) cells involved in both humoral and cell-mediated responses (Miyata & Van-Eeden 2011). The other endpoints evaluated here, i.e.…”

Tumor Necrosis Factor-Alpha as Biomarkers of Exposure to Indoor Pollutants Among Primary School Children in Klang Valley

“…School children living in urban area which are exposed to high concentration of indoor air pollutants significantly have a high level of TNF-α. This might indicate that urban school exposed to traffic emission are more polluted, leading TNF-α in lung to play a critical role in mediating inflammatory cell recruitment after exposure to particulate matters (Miyata and Van Eeden, 2011). Activated macrophages in human lung provide protection against infections by a variety of mechanisms including cytokine production (particularly IL-1, IL-6 and IL-8, also TNF-α), which are important in mounting an immune response to infection (Barnes, 2009).…”

Impact of Particulate Matter Exposition on the Risk of Ischemic Stroke: Epidemiologic Evidence and Putative Mechanisms

“…41 Subsequently, ROSreleasing enzymes such as nicotinamide adenine dinucleotide phosphate-oxidase oxidase are activated, and proinflammatory cytokines such as interleukin 6 are released. [41][42][43] Large fractions of PM, e.g. transition metals, oxidize phospholipids (surfactants) in the lungs.…”

“…[41][42][43] Oxidized surfactants in turn are ligands for toll-like receptor and scavenger receptor. [41][42][43] This activation of the local pulmonary innate immune system leads to a powerful burst of ROS and proinflammatory markers within the lung parenchyma. In addition, up to 80% of PM, predominantly the coarse fraction, is able to enter pulmonary parenchyma by transcytosis through macrophages and alveolar epithelium cells.…”

“…44 As a consequence, the occurrence of these PM-protein complexes in pulmonary and systemic circulations can induce systemic immune responses, particularly in adipose tissue. 43,44 In summary, PM exposure is capable of triggering a complex immune response, which is initiated locally in the lung parenchyma and which subsequently activates systemic proinflammatory cascades (Figure 1). Both mechanisms, the proinflammatory reaction of the lungs and the translocation of particles to other organs, are thought to be responsible for the endothelial dysfunction after PM exposure.…”