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Systemic inflammation after inspiratory loading in chronic obstructive pulmonary disease

OBJECTIVE: Patients with chronic obstructive pulmonary disease (COPD) present systemic inflammation. Strenuous resistive breathing induces systemic inflammation in healthy subjects. We hypothesized that the increased respiratory load that characterizes COPD can contribute to systemic inflammation in...

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Detalles Bibliográficos
Autores principales: Fuster, Antonia, Sauleda, Jaume, Sala, Ernest, Barceló, Bernardí, Pons, Jaume, Carrera, Miguel, Noguera, Aina, Togores, Bernat, Agustí, Alvar GN
Formato: Texto
Lenguaje:English
Publicado: Dove Medical Press 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2528210/
https://www.ncbi.nlm.nih.gov/pubmed/18488438
Descripción
Sumario:OBJECTIVE: Patients with chronic obstructive pulmonary disease (COPD) present systemic inflammation. Strenuous resistive breathing induces systemic inflammation in healthy subjects. We hypothesized that the increased respiratory load that characterizes COPD can contribute to systemic inflammation in these patients. PATIENTS AND METHODS: To test this hypothesis, we compared leukocyte numbers and levels of circulating cytokines (tumor necrosis factor alpha [TNFα], interleukin-1β [IL-1β], IL-6, IL-8, and IL-10), before and 1 hour after maximal incremental inspiratory loading in 13 patients with stable COPD (forced expiratory volume in one second [FEV(1)] 29 ± 2.5% ref) and in 8 healthy sedentary subjects (FEV(1) 98 ± 5% ref). RESULTS: We found that: (1) at baseline, patients with COPD showed higher leukocyte counts and IL-8 levels than controls (p < 0.01); and, (2) one hour after maximal inspiratory loading these values were unchanged, except for IL-10, which increased in controls (p < 0.05) but not in patients with COPD. CONCLUSIONS: This study confirms the presence of systemic inflammation in COPD, shows that maximal inspiratory loading does not increase the levels of pro-inflammatory cytokines (IL-1β, IL-8) in COPD patients or controls, but suggests that the former may be unable to mount an appropriate systemic anti-inflammatory response to exercise.