Beware, pneumonia is in the air

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Science Translational Medicine  10 Jun 2015:
Vol. 7, Issue 291, pp. 291ec95
DOI: 10.1126/scitranslmed.aac5094

Exposure to household air pollution (HAP) in the form of biomass fuel smoke increases the risk of pneumonia, especially for children. A notable proportion of the world’s population residing in low- and middle-income countries experience exposure to biomass fuel on a daily basis, resulting in ~1 million surplus deaths per year compared with unexposed individuals. Rylance et al. investigated the mechanisms underlying smoke-related risks for pulmonary infection and chronic disease because understanding such mechanisms could improve strategies to prevent pneumonia in countries using biomass fuel. Specific issues addressed by this study were (i) the reliability of a monocyte-derived macrophage (MDM) model compared with observed in vivo responses of human alveolar macrophages (HAMs) to smoke exposure; (ii) the effect of particulates on the function of HAMs, including cytokine production, phagocytosis, oxidative burst, and pathogen killing; and (iii) the impact of different wood and particle types.

Bronchoalveolar lavage (BAL) was performed to obtain HAMs from healthy Malawian adults naturally exposed to HAP. The authors microscopically assessed the particulate load of the HAMs from individuals exposed to HAP and tested the macrophages’ capacity for burst oxidation. In addition, HAMs from unexposed healthy controls from Liverpool were compared with human MDMs in vitro to evaluate the responses of cells to particulates of respirable size. Exposure time and doses were adjusted to ensure that the in vitro experiments yielded similar microscopic appearances to the samples obtained by BAL from HAP-exposed Malawian participants. Cellular inflammatory response to particulate challenge was evaluated by measuring interleukin (IL)-6 and IL-8 production, and the uptake and oxidation of fluorescence-labeled beads were used to assess phagocytic function. The ingestion and killing of Streptococcus pneumoniae and Mycobacterium tuberculosis were measured by microscopy and quantitative culture. Last, particulate ingestion was quantified by digital image analysis. Two different wood types (Malawian cooking wood and Norwegian birch wood) were used to determine whether there would be a difference in the effects related to smoke particulate from different sources. The investigators demonstrated that human MDMs challenged with smoke ex vivo are similar to HAMs exposed to household air pollution (HAP) in vivo. Oxidative burst activity was decreased in HAP-exposed Malawians with HAMs containing more particulate matter. In addition, they demonstrated a dose-related increase in cytokine production and decrease in phagocytosis and oxidative burst function in response to smoke exposure. The researchers thus inferred that particulate loading of alveolar macrophages could serve as a marker of macrophage functional impairment and provide a link between HAP and respiratory infection. The particulate content of MDMs was negatively correlated with phagocytosis rate, and Malawian wood was noted to have the greatest inhibitory effect.

The observations in this study suggest that defects in the pulmonary innate immune system resulting from HAP exposure impair alveolar macrophage-mediated defenses against common pathogens found in the lower respiratory tract, increasing the risk of pneumonia. These findings align with observations from clinical and epidemiological studies that associate respiratory tract infections and HAP.

J. Rylance et al., Household air pollution causes dose-dependent inflammation and altered phagocytosis in human macrophages. Am. J. Respir. Cell Mol. Biol. 52, 584–593 (2015). [Abstract]

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