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

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• dc.contributor.author Farré López, Núriaca
• dc.contributor.author Farré, Ramonca
• dc.contributor.author Gozal, Davidca
• dc.date.accessioned 2018-10-24T07:40:31Z
• dc.date.issued 2018
• dc.description.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.
• dc.format.mimetype application/pdf
• dc.identifier.citation Farré N, Farré R, Gozal D. Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?. Chest. 2018 Oct;154(4):754-759. DOI: 10.1016/j.chest.2018.03.001
• dc.identifier.doi http://dx.doi.org/10.1016/j.chest.2018.03.001
• dc.identifier.issn 0012-3692
• dc.identifier.uri http://hdl.handle.net/10230/35640
• dc.language.iso eng
• dc.publisher Elsevierca
• dc.relation.ispartof Chest. 2018 Oct;154(4):754-9
• dc.rights © Elsevier http://dx.doi.org/10.1016/j.chest.2018.03.001
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.subject.keyword Commentary
• dc.subject.keyword Intermittent hypoxia
• dc.subject.keyword Microbiome
• dc.subject.keyword Sleep apnea
• dc.subject.keyword Sleep fragmentation
• dc.subject.other Son -- Aspectes fisiològics
• dc.subject.other Trastorns del son
• dc.title Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?ca
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/acceptedVersion