Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?
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 ai...
| Autores: | , , |
|---|---|
| Formato: | artículo |
| Estado: | Versión aceptada para publicación |
| Fecha de publicación: | 2018 |
| País: | España |
| Recursos: | Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
| Repositorio: | Recercat. Dipósit de la Recerca de Catalunya |
| OAI Identifier: | oai:recercat.cat:10230/35640 |
| Acesso em linha: | http://hdl.handle.net/10230/35640 http://dx.doi.org/10.1016/j.chest.2018.03.001 |
| Access Level: | acceso abierto |
| Palavra-chave: | Son -- Aspectes fisiològics Trastorns del son Commentary Intermittent hypoxia Microbiome Sleep apnea Sleep fragmentation |
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Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?Farré López, NúriaFarré, RamonGozal, DavidSon -- Aspectes fisiològicsTrastorns del sonCommentaryIntermittent hypoxiaMicrobiomeSleep apneaSleep fragmentationOSA 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.Elsevier20182018info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfapplication/pdfhttp://hdl.handle.net/10230/35640http://dx.doi.org/10.1016/j.chest.2018.03.001reponame:Recercat. Dipósit de la Recerca de Catalunyainstname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya)InglésChest. 2018 Oct;154(4):754-9© Elsevier http://dx.doi.org/10.1016/j.chest.2018.03.001info:eu-repo/semantics/openAccessoai:recercat.cat:10230/356402026-05-29T05:05:01Z |
| dc.title.none.fl_str_mv |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| title |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| spellingShingle |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? Farré López, Núria Son -- Aspectes fisiològics Trastorns del son Commentary Intermittent hypoxia Microbiome Sleep apnea Sleep fragmentation |
| title_short |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| title_full |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| title_fullStr |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| title_full_unstemmed |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| title_sort |
Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk? |
| dc.creator.none.fl_str_mv |
Farré López, Núria Farré, Ramon Gozal, David |
| author |
Farré López, Núria |
| author_facet |
Farré López, Núria Farré, Ramon Gozal, David |
| author_role |
author |
| author2 |
Farré, Ramon Gozal, David |
| author2_role |
author author |
| dc.subject.none.fl_str_mv |
Son -- Aspectes fisiològics Trastorns del son Commentary Intermittent hypoxia Microbiome Sleep apnea Sleep fragmentation |
| topic |
Son -- Aspectes fisiològics Trastorns del son Commentary Intermittent hypoxia Microbiome Sleep apnea Sleep fragmentation |
| description |
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. |
| publishDate |
2018 |
| dc.date.none.fl_str_mv |
2018 2018 |
| dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/acceptedVersion |
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article |
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acceptedVersion |
| dc.identifier.none.fl_str_mv |
http://hdl.handle.net/10230/35640 http://dx.doi.org/10.1016/j.chest.2018.03.001 |
| url |
http://hdl.handle.net/10230/35640 http://dx.doi.org/10.1016/j.chest.2018.03.001 |
| dc.language.none.fl_str_mv |
Inglés |
| language_invalid_str_mv |
Inglés |
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Chest. 2018 Oct;154(4):754-9 |
| dc.rights.none.fl_str_mv |
© Elsevier http://dx.doi.org/10.1016/j.chest.2018.03.001 info:eu-repo/semantics/openAccess |
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© Elsevier http://dx.doi.org/10.1016/j.chest.2018.03.001 |
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openAccess |
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application/pdf application/pdf |
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Elsevier |
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Elsevier |
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reponame:Recercat. Dipósit de la Recerca de Catalunya instname:Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
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Varias* (Consorci de Biblioteques Universitáries de Catalunya, Centre de Serveis Científics i Acadèmics de Catalunya) |
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Recercat. Dipósit de la Recerca de Catalunya |
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