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Chest. 2018 Oct;154(4):754-759. doi: 10.1016/j.chest.2018.03.001. Epub 2018 Mar 14.

Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?

Author information

1
Heart Failure Programme, Department of Cardiology, Hospital del Mar, Barcelona, Heart Diseases Biomedical Research Group, IMIM (Hospital del Mar Medical Research Institute), Barcelona, and the Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
2
Unitat de Biofísica i Bioenginyeria, Facultat de Medicina i Ciències de la Salut, Universitat de Barcelona-IDIBAPS, Barcelona, and CIBER de Enfermedades Respiratorias, Madrid, Spain.
3
Section of Pediatric Sleep Medicine, Department of Pediatrics, Biological Sciences Division, The University of Chicago, Chicago, IL. Electronic address: dgozal@uchicago.edu.

Abstract

OSA has emerged as a highly prevalent public health problem that imposes important mid- and long-term consequences, namely cardiovascular, metabolic, cognitive, and cancer-related alterations. OSA is characterized by increased upper airway resistance, alveolar hypoventilation, and recurrent upper airway obstruction during sleep. Recurrent collapse of the upper airway develops with sleep onset and is associated with both intermittent hypoxemia and sleep fragmentation. The microbiome is a vast and complex polymicrobial ecosystem that coexists with the human organism, and it has been identified as playing significant roles in the development of host immunologic phenotypes. In humans and animal models, changes in gut microbial communities occur with lifestyle behaviors, such as smoking, long-distance travel, dietary preferences, physical exercise, and circadian rhythm disturbances. In parallel, diseases previously attributed in part to lifestyle such as obesity, coronary heart disease, depression, and asthma (also associated with OSA) are now claimed as microbiota related. We therefore posit that altered patterns of sleep and oxygenation, as seen in OSA, will promote specific alterations in gut microbiota that in turn will elicit the immunologic alterations that lead to OSA-induced end-organ morbidities. The present article assesses the potential mechanistic links between OSA-induced changes in gut microbiota and its morbid phenotypes.

KEYWORDS:

commentary; intermittent hypoxia; microbiome; sleep apnea; sleep fragmentation

PMID:
29548630
DOI:
10.1016/j.chest.2018.03.001
[Indexed for MEDLINE]

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