Effects of carbon black particles on human monocyte-derived macrophages: type-dependent pro-inflammatory activation in vitro.

Abstract

Carbon black is a key component of air-borne particulate matter, linked to adverse health outcomes, such as increased susceptibility to respiratory infections and chronic pulmonary disease exacerbations. Fine and ultrafine particles can penetrate the lungs, enter the bloodstream, and induce pathogenetic events. Macrophages play a crucial role in responding to inhaled particles, including carbon black, by initiating an innate immune response and upregulating pro-inflammatory cytokines and anti-oxidative enzymes. This study investigates the effects of carbon black particles on human monocyte-derived macrophages in vitro at a concentration of 10 µg/ml, offering insights into their potential role in disease pathogenesis. We have compared two commercially available carbon black particle types using various physicochemical techniques and assessed their biological effects on monocyte-derived macrophages. We have evaluated changes in cell viability, morphology, and particle uptake/phagocytosis. Western blot, ELISA, and RT-qPCR measured inflammatory and oxidative stress biomarkers. Both types of carbon black particles induced similar responses in macrophages, including particle uptake, cytokine production, and oxidative stress-related protein expression. The observed changes suggest activation of the Nrf2-mediated antioxidant response, impaired autophagy, and decreased cellular defense against oxidative stress, indicating potential pathways for chronic inflammatory lung disease development.