Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity

Martha Torres, Claudia Carranza, Srijata Sarkar, Yolanda Gonzalez, Alvaro Osornio Vargas, Kathleen Black, Qingyu Meng, Raul Quintana-Belmares, Martha Hernandez, Jose Juan F. Angeles Garcia, Victor Hugo Páramo-Figueroa, Marco Antonio Iñiguez-Garcia, Jose L. Flores, Junfeng Zhang, Carol R. Gardner, Pamela Ohman Strickland, Stephan Schwander

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Rationale Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored. Objectives To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM 2.5 (< 2.5 μm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis. Methods Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM 2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis. Measurements and main results In vitro exposure of AM to PM 2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-i 3) in BAC, and negatively correlated with PPD-induced IFN-γin PBMC. Conclusions Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.

Original languageEnglish (US)
Pages (from-to)675-683
Number of pages9
JournalThorax
Volume74
Issue number7
DOIs
StatePublished - Jul 1 2019

Fingerprint

Particulate Matter
Mycobacterium tuberculosis
Immunity
Lung
Alveolar Macrophages
Blood Cells
Cytokines
Mexico
Phagocytosis
Inhalation Exposure
Air Pollution
Interleukin-1
Interferon-gamma
Microscopy
Flow Cytometry
Proteins
Tumor Necrosis Factor-alpha

All Science Journal Classification (ASJC) codes

  • Pulmonary and Respiratory Medicine

Keywords

  • alveolar macrophages
  • particulate matter
  • pollution
  • tuberculosis

Cite this

Torres, Martha ; Carranza, Claudia ; Sarkar, Srijata ; Gonzalez, Yolanda ; Osornio Vargas, Alvaro ; Black, Kathleen ; Meng, Qingyu ; Quintana-Belmares, Raul ; Hernandez, Martha ; Angeles Garcia, Jose Juan F. ; Páramo-Figueroa, Victor Hugo ; Iñiguez-Garcia, Marco Antonio ; Flores, Jose L. ; Zhang, Junfeng ; Gardner, Carol R. ; Ohman Strickland, Pamela ; Schwander, Stephan. / Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity. In: Thorax. 2019 ; Vol. 74, No. 7. pp. 675-683.
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title = "Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity",
abstract = "Rationale Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored. Objectives To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM 2.5 (< 2.5 μm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis. Methods Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM 2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis. Measurements and main results In vitro exposure of AM to PM 2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-i 3) in BAC, and negatively correlated with PPD-induced IFN-γin PBMC. Conclusions Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.",
keywords = "alveolar macrophages, particulate matter, pollution, tuberculosis",
author = "Martha Torres and Claudia Carranza and Srijata Sarkar and Yolanda Gonzalez and {Osornio Vargas}, Alvaro and Kathleen Black and Qingyu Meng and Raul Quintana-Belmares and Martha Hernandez and {Angeles Garcia}, {Jose Juan F.} and P{\'a}ramo-Figueroa, {Victor Hugo} and I{\~n}iguez-Garcia, {Marco Antonio} and Flores, {Jose L.} and Junfeng Zhang and Gardner, {Carol R.} and {Ohman Strickland}, Pamela and Stephan Schwander",
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Torres, M, Carranza, C, Sarkar, S, Gonzalez, Y, Osornio Vargas, A, Black, K, Meng, Q, Quintana-Belmares, R, Hernandez, M, Angeles Garcia, JJF, Páramo-Figueroa, VH, Iñiguez-Garcia, MA, Flores, JL, Zhang, J, Gardner, CR, Ohman Strickland, P & Schwander, S 2019, 'Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity', Thorax, vol. 74, no. 7, pp. 675-683. https://doi.org/10.1136/thoraxjnl-2018-212529

Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity. / Torres, Martha; Carranza, Claudia; Sarkar, Srijata; Gonzalez, Yolanda; Osornio Vargas, Alvaro; Black, Kathleen; Meng, Qingyu; Quintana-Belmares, Raul; Hernandez, Martha; Angeles Garcia, Jose Juan F.; Páramo-Figueroa, Victor Hugo; Iñiguez-Garcia, Marco Antonio; Flores, Jose L.; Zhang, Junfeng; Gardner, Carol R.; Ohman Strickland, Pamela; Schwander, Stephan.

In: Thorax, Vol. 74, No. 7, 01.07.2019, p. 675-683.

Research output: Contribution to journalArticle

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T1 - Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity

AU - Torres, Martha

AU - Carranza, Claudia

AU - Sarkar, Srijata

AU - Gonzalez, Yolanda

AU - Osornio Vargas, Alvaro

AU - Black, Kathleen

AU - Meng, Qingyu

AU - Quintana-Belmares, Raul

AU - Hernandez, Martha

AU - Angeles Garcia, Jose Juan F.

AU - Páramo-Figueroa, Victor Hugo

AU - Iñiguez-Garcia, Marco Antonio

AU - Flores, Jose L.

AU - Zhang, Junfeng

AU - Gardner, Carol R.

AU - Ohman Strickland, Pamela

AU - Schwander, Stephan

PY - 2019/7/1

Y1 - 2019/7/1

N2 - Rationale Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored. Objectives To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM 2.5 (< 2.5 μm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis. Methods Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM 2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis. Measurements and main results In vitro exposure of AM to PM 2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-i 3) in BAC, and negatively correlated with PPD-induced IFN-γin PBMC. Conclusions Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.

AB - Rationale Associations between urban (outdoor) airborne particulate matter (PM) exposure and TB and potential biological mechanisms are poorly explored. Objectives To examine whether in vivo exposure to urban outdoor PM in Mexico City and in vitro exposure to urban outdoor PM 2.5 (< 2.5 μm median aerodynamic diameter) alters human host immune cell responses to Mycobacterium tuberculosis. Methods Cellular toxicity (flow cytometry, proliferation assay (MTS assay)), M. tuberculosis and PM 2.5 phagocytosis (microscopy), cytokine-producing cells (Enzyme-linked immune absorbent spot (ELISPOT)), and signalling pathway markers (western blot) were examined in bronchoalveolar cells (BAC) and peripheral blood mononuclear cells (PBMC) from healthy, non-smoking, residents of Mexico City (n=35; 13 female, 22 male). In vivo-acquired PM burden in alveolar macrophages (AM) was measured by digital image analysis. Measurements and main results In vitro exposure of AM to PM 2.5 did not affect M. tuberculosis phagocytosis. High in vivo-acquired AM PM burden reduced constitutive, M. tuberculosis and PM-induced interleukin-1β production in freshly isolated BAC but not in autologous PBMC while it reduced constitutive production of tumour necrosis factor-alpha in both BAC and PBMC. Further, PM burden was positively correlated with constitutive, PM, M. tuberculosis and purified protein derivative (PPD)-induced interferon gamma (IFN-i 3) in BAC, and negatively correlated with PPD-induced IFN-γin PBMC. Conclusions Inhalation exposure to urban air pollution PM impairs important components of the protective human lung and systemic immune response against M. tuberculosis. PM load in AM is correlated with altered M. tuberculosis-induced cytokine production in the lung and systemic compartments. Chronic PM exposure with high constitutive expression of proinflammatory cytokines results in relative cellular unresponsiveness.

KW - alveolar macrophages

KW - particulate matter

KW - pollution

KW - tuberculosis

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Torres M, Carranza C, Sarkar S, Gonzalez Y, Osornio Vargas A, Black K et al. Urban airborne particle exposure impairs human lung and blood Mycobacterium tuberculosis immunity. Thorax. 2019 Jul 1;74(7):675-683. https://doi.org/10.1136/thoraxjnl-2018-212529