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Exercise-induced alterations in phospholipid hydrolysis, airway surfactant, and eicosanoids and their role in airway hyperresponsiveness in asthma.
Murphy, Ryan C; Lai, Ying; Nolin, James D; Aguillon Prada, Robier A; Chakrabarti, Arindam; Novotny, Michael V; Seeds, Michael C; Altemeier, William A; Gelb, Michael H; Hite, Robert Duncan; Hallstrand, Teal S.
Afiliación
  • Murphy RC; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington.
  • Lai Y; Center for Lung Biology, University of Washington, Seattle, Washington.
  • Nolin JD; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington.
  • Aguillon Prada RA; Center for Lung Biology, University of Washington, Seattle, Washington.
  • Chakrabarti A; Division of Pulmonary, Critical Care, and Sleep Medicine, Department of Medicine, University of Washington, Seattle, Washington.
  • Novotny MV; Center for Lung Biology, University of Washington, Seattle, Washington.
  • Seeds MC; Department of Critical Care, Cleveland Clinic, Cleveland, Ohio.
  • Altemeier WA; Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio.
  • Gelb MH; Department of Critical Care, Cleveland Clinic, Cleveland, Ohio.
  • Hite RD; Department of Pathobiology, Cleveland Clinic, Cleveland, Ohio.
  • Hallstrand TS; Department of Critical Care, Cleveland Clinic, Cleveland, Ohio.
Am J Physiol Lung Cell Mol Physiol ; 320(5): L705-L714, 2021 05 01.
Article en En | MEDLINE | ID: mdl-33533300
ABSTRACT
The mechanisms responsible for driving endogenous airway hyperresponsiveness (AHR) in the form of exercise-induced bronchoconstriction (EIB) are not fully understood. We examined alterations in airway phospholipid hydrolysis, surfactant degradation, and lipid mediator release in relation to AHR severity and changes induced by exercise challenge. Paired induced sputum (n = 18) and bronchoalveolar lavage (BAL) fluid (n = 11) were obtained before and after exercise challenge in asthmatic subjects. Samples were analyzed for phospholipid structure, surfactant function, and levels of eicosanoids and secreted phospholipase A2 group 10 (sPLA2-X). A primary epithelial cell culture model was used to model effects of osmotic stress on sPLA2-X. Exercise challenge resulted in increased surfactant degradation, phospholipase activity, and eicosanoid production in sputum samples of all patients. Subjects with EIB had higher levels of surfactant degradation and phospholipase activity in BAL fluid. Higher basal sputum levels of cysteinyl leukotrienes (CysLTs) and prostaglandin D2 (PGD2) were associated with direct AHR, and both the postexercise and absolute change in CysLTs and PGD2 levels were associated with EIB severity. Surfactant function either was abnormal at baseline or became abnormal after exercise challenge. Baseline levels of sPLA2-X in sputum and the absolute change in amount of sPLA2-X with exercise were positively correlated with EIB severity. Osmotic stress ex vivo resulted in movement of water and release of sPLA2-X to the apical surface. In summary, exercise challenge promotes changes in phospholipid structure and eicosanoid release in asthma, providing two mechanisms that promote bronchoconstriction, particularly in individuals with EIB who have higher basal levels of phospholipid turnover.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fosfolípidos / Hipersensibilidad Respiratoria / Asma / Tensoactivos / Ejercicio Físico / Eicosanoides / Fosfolipasas A2 Grupo X Límite: Adolescent / Adult / Female / Humans / Male Idioma: En Revista: Am J Physiol Lung Cell Mol Physiol Asunto de la revista: BIOLOGIA MOLECULAR / FISIOLOGIA Año: 2021 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fosfolípidos / Hipersensibilidad Respiratoria / Asma / Tensoactivos / Ejercicio Físico / Eicosanoides / Fosfolipasas A2 Grupo X Límite: Adolescent / Adult / Female / Humans / Male Idioma: En Revista: Am J Physiol Lung Cell Mol Physiol Asunto de la revista: BIOLOGIA MOLECULAR / FISIOLOGIA Año: 2021 Tipo del documento: Article