Low-Dose oxygen enhances macrophage-derived bacterial clearance following cigarette smoke exposure

William G. Bain, Ashutosh Tripathi, Pooja Mandke, Jonathan H. Gans, Franco D'Alessio, Venkataramana Sidhaye, Neil R. Aggarwal

Research output: Contribution to journalArticle

Abstract

Background. Chronic obstructive pulmonary disease (COPD) is a common, smoking-related lung disease. Patients with COPD frequently suffer disease exacerbations induced by bacterial respiratory infections, suggestive of impaired innate immunity. Low-dose oxygen is a mainstay of therapy during COPD exacerbations; yet we understand little about whether oxygen can modulate the effects of cigarette smoke on lung immunity. Methods. Wild-type mice were exposed to cigarette smoke for 5 weeks, followed by intratracheal instillation of Pseudomonas aeruginosa (PAO1) and 21% or 35-40% oxygen. After two days, lungs were harvested for PAO1 CFUs, and bronchoalveolar fluid was sampled for inflammatory markers. In culture, macrophages were exposed to cigarette smoke and oxygen (40%) for 24 hours and then incubated with PAO1, followed by quantification of bacterial phagocytosis and inflammatory markers. Results. Mice exposed to 35-40% oxygen after cigarette smoke and PAO1 had improved survival and reduced lung CFUs and inflammation. Macrophages from these mice expressed less TNF and more scavenger receptors. In culture, macrophages exposed to cigarette smoke and oxygen also demonstrated decreased TNF secretion and enhanced phagocytosis of PAO1 bacteria. Conclusions. Our findings demonstrate a novel, protective role for low-dose oxygen following cigarette smoke and bacteria exposure that may be mediated by enhanced macrophage phagocytosis.

Original languageEnglish (US)
Article number1280347
JournalJournal of Immunology Research
Volume2016
DOIs
StatePublished - 2016

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Smoke
Tobacco Products
Macrophages
Oxygen
Phagocytosis
Chronic Obstructive Pulmonary Disease
Disease Progression
Bacteria
Scavenger Receptors
Lung
Bacterial Infections
Innate Immunity
Respiratory Tract Infections
Pseudomonas aeruginosa
Lung Diseases
Immunity
Pneumonia
Smoking
Survival

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

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Low-Dose oxygen enhances macrophage-derived bacterial clearance following cigarette smoke exposure. / Bain, William G.; Tripathi, Ashutosh; Mandke, Pooja; Gans, Jonathan H.; D'Alessio, Franco; Sidhaye, Venkataramana; Aggarwal, Neil R.

In: Journal of Immunology Research, Vol. 2016, 1280347, 2016.

Research output: Contribution to journalArticle

Bain, William G. ; Tripathi, Ashutosh ; Mandke, Pooja ; Gans, Jonathan H. ; D'Alessio, Franco ; Sidhaye, Venkataramana ; Aggarwal, Neil R. / Low-Dose oxygen enhances macrophage-derived bacterial clearance following cigarette smoke exposure. In: Journal of Immunology Research. 2016 ; Vol. 2016.
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abstract = "Background. Chronic obstructive pulmonary disease (COPD) is a common, smoking-related lung disease. Patients with COPD frequently suffer disease exacerbations induced by bacterial respiratory infections, suggestive of impaired innate immunity. Low-dose oxygen is a mainstay of therapy during COPD exacerbations; yet we understand little about whether oxygen can modulate the effects of cigarette smoke on lung immunity. Methods. Wild-type mice were exposed to cigarette smoke for 5 weeks, followed by intratracheal instillation of Pseudomonas aeruginosa (PAO1) and 21{\%} or 35-40{\%} oxygen. After two days, lungs were harvested for PAO1 CFUs, and bronchoalveolar fluid was sampled for inflammatory markers. In culture, macrophages were exposed to cigarette smoke and oxygen (40{\%}) for 24 hours and then incubated with PAO1, followed by quantification of bacterial phagocytosis and inflammatory markers. Results. Mice exposed to 35-40{\%} oxygen after cigarette smoke and PAO1 had improved survival and reduced lung CFUs and inflammation. Macrophages from these mice expressed less TNF and more scavenger receptors. In culture, macrophages exposed to cigarette smoke and oxygen also demonstrated decreased TNF secretion and enhanced phagocytosis of PAO1 bacteria. Conclusions. Our findings demonstrate a novel, protective role for low-dose oxygen following cigarette smoke and bacteria exposure that may be mediated by enhanced macrophage phagocytosis.",
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