Adverse effects of wood smoke PM_2.5exposure on macrophage functions

Abstract

Epidemiological studies have shown a correlation between chronic biomass smoke exposure and increased respiratory infection. Pulmonary macrophages are instrumental in both the innate and the adaptive immune responses to respiratory infection. In the present study, in vitro systems were utilized where alveolar macrophages (AM) and bone marrow-derived macrophages (BMdM) were exposed to concentrated wood smoke-derived particulate matter (WS-PM) and mice were exposed in vivo to either concentrated WS-PM or inhaled WS. In vivo studies demonstrated that WS-exposed mice inoculated with Streptococcus pneumoniae had a higher bacterial load 24 h post-exposure, and corresponding AM were found to have decreased lymphocyte activation activity. Additionally, while classic markers of inflammation (cellular infiltration, total protein, neutrophils) were not affected, there were changes in pulmonary macrophages populations, including significant decreases in macrophages expressing markers of activation in WS-exposed mice. The lymphocyte activation activity of WS-PM-exposed AM was significantly suppressed, but the phagocytic activity appeared unchanged. In an effort to determine a pathway for WS-induced suppression, RelB activation, assessed by nuclear translocation, was observed in AM exposed to either inhaled WS or instilled WS-PM. Finally, an analysis of WS-PM fractions determined the presence of 4–5 polycyclic aromatic hydrocarbons (PAHs), and preliminary work suggests a potential role for these PAHs to alter macrophage functions. These studies show a decreased ability of WS-exposed pulmonary macrophages to effectively mount a defense against infection, the effect lasts at least a week post-exposure, and appears to be mediated via RelB activation.

Respiratory risks from household air pollution in low and middle income countries

“…In rats, the lung shows minor pulmonary inflammation and reduced interleukin-1β after 70 days of in-vivo HAP exposure 73. Similar findings of reduced release of interleukin-8 by ex-vivo alveolar macrophages at baseline, and after further challenge with wood smoke particles, have been seen in human beings exposed to HAP 72,74. Adequate cytokine and chemokine responses are important for neutrophil recruitment 75.…”

“…The little evidence available for subacute and chronic HAP exposure (in vivo) suggests that compensatory changes limit inflammatory responses in mice, with lower interferon-γ response in T-cell co-culture 7 days after exposure to wood smoke 72. In rats, the lung shows minor pulmonary inflammation and reduced interleukin-1β after 70 days of in-vivo HAP exposure 73.…”

Comparison of in vitro toxicological effects of biomass smoke from different sources of animal dung

“…AhR and JNK-AP-1 activation has also been reported in submerged cultures of lung cells exposed to other types of biomass smoke. Migliaccio et al showed that mouse monocytes treated with particulate matter from wood smoke had increased expression of an AhR-regulated gene, and Martey et al found that human lung fibroblasts exposed to tobacco smoke extract displayed AhR nuclear translocation (31, 53). Additionally, increased levels of phosphorylated JNK were observed in human bronchial epithelial cells treated with wood smoke extract (26).…”

Health impacts of anthropogenic biomass burning in the developed world

“…In mice and rats, long-term inhalation of woodsmoke in concentrations relevant for ambient exposure induces mild inflammatory effects in the airways, systemic inflammation and decreased lung function [17,[108][109][110][111][112]. Woodsmoke PM has also been reported to exacerbate allergic inflammation and allergic sensitisation, and to decrease pulmonary macrophage function in terms of impaired infection resistance [17,109,[112][113][114], this was recently demonstrated to apply equally to particles from Malawian and Norwegian woodsmoke [115]. Overall, in vivo and in vitro experiments demonstrate that woodsmoke PM can induce inflammatory responses, cytotoxicity, genotoxicity, oxidative stress and immunosuppressive effects [17, 93-95, 104, 111, 116-122].…”