Exposure of murine macrophages to carbon nanoparticles promotes inflammation and inhibits phagocytosis (130.5)

Abstract

Abstract Exposure to respirable ultrafine particles (2.5 μM) can adversely affect human health and have been implicated with episodes of increased respiratory diseases such as asthma and allergies; the same is predicted for nanoparticles, which can reach deeper regions of the lung. The objective of this investigation was to examine the effects of carbon nanoparticles on alveolar macrophages. Macrophages (MΦ) function as the first line of defense against invading pathogens and are likely to be amongst the first cells affected by nanoparticulates. We focused on two manufactured nanoparticles: multiwalled carbon nanotube aggregates and black-carbon. The two were tested against MΦ in a chronic contact model. We hypothesized that exposure to nanoparticles would decrease MΦ ability to effectively respond to immunological challenge. Production of interleukin (IL)-12 and nitric oxide (NO), as well as phagocytosis, and MΦ activation were examined in response to lipopolysaccharide (LPS) following a 144 hr exposure to the nanoparticles. Data demonstrated an increase in NO and IL-12 production, a decrease in phagocytosis, and a decrease in the expression levels of activation markers. The data suggests that carbon nanoparticle exposure alters MΦ responses to LPS marked by increased inflammation while potentially limiting clearance and ability to interact with effector T-cells. Thus, physiological exposure to carbon nanoparticles could potentially lead to ineffective pulmonary immunity.