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Diffuse Lung Disease |

Macrophage Exposure to Wood Smoke Increases Susceptibility to Develop Pulmonary Tuberculosis

Isabel Sada-Ovalle, PhD; Leslie Chavéz-Galán, PhD; Stephanie Aldrighetti, MS; Luis Torre-Bouscoulet, MD; Rosario Fernández Plata, MS; Rogelio Pérez Padilla, MD; Irma Rosas, PhD
Author and Funding Information

Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico Distrito Federal, Mexico


Chest. 2013;144(4_MeetingAbstracts):479A. doi:10.1378/chest.1703843
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Abstract

SESSION TITLE: Occupational/ Environmental Lung Disease Posters

SESSION TYPE: Original Investigation Poster

PRESENTED ON: Wednesday, October 30, 2013 at 01:30 PM - 02:30 PM

PURPOSE: Combustion of biomass and wood can result in the generation of many toxic compounds including polycyclic aromatic hydrocarbons (PAH) that increases the risk of chronic obstructive pulmonary disease, lung cancer and pulmonary tuberculosis (PTB). The association between chronic wood smoke exposure and PTB has been previously demonstrated. Alveolar macrophages (AM) are the principle cells that process airborne particles and pathogens in the lung such as Mycobacterium tuberculosis (Mtb). In the present study we used an in vitro experimental system to analyze the immunological association between macrophage pre-exposure to organic extracts (PHA) from wood smoke and macrophage ability to control intracellular bacterial growth.

METHODS: Wood smoke was collected with a PM10 high volume air sampler from a wood stove and from a rural area in Mexico. Organic extracts were recovered by shaking the samples with dichloromethane and characterized by GC/MS. Monocyte derived macrophages (MDM) from healthy donors or THP-macrophages (THP1) were exposed for 24 hr to 1, 5 or 10 μg/mL of PAH and then infected with Mtb for 2 hr. Four days after infection, cells were lysed and mycobacteria enumerated. Crystalline silica was used as a positive control. Expression of cell surface markers and cell death (apoptosis) were analyzed by flow cytometry.

RESULTS: Twenty one PAH were identified (benz[a]anthracene, fluoranthene, pyrene, etc.) as part of the organic extracts. Pre-exposure of MDM and THP macrophages to PAH limited in a dose-dependent manner the macrophage ability to control of intracellular bacterial growth. Next, we analyzed the expression of cell surface markers and identified that TLR2 expression was diminished in a dose-dependent manner but the expression of IL-1 and TNF-alpha receptors was increased. PAH generated mitochondrial damage and induced more apoptosis in pre-exposed macrophages than that observed in unexposed macrophages.

CONCLUSIONS: Our results suggest that organic extracts (PAH) collected from wood smoke sensitizes macrophages to present cell death and this deregulation of cell death balance may be detrimental to the host defenses because it could favor the release of viable mycobacteria and; therefore of pulmonary tuberculosis.

CLINICAL IMPLICATIONS: We provide scientific evidence to community leaders and policy makers about the impact of exposure to biomass fuels and the risk for development of tuberculosis to implement interventions that decrease the use of biomass fuels in poor communities.

DISCLOSURE: The following authors have nothing to disclose: Isabel Sada-Ovalle, Leslie Chavéz-Galán, Stephanie Aldrighetti, Luis Torre-Bouscoulet, Rosario Fernández Plata, Rogelio Pérez Padilla, Irma Rosas

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