Sleep deprivation predisposes allergic mice to neutrophilic lung inflammation - 07/03/18
, Daniela S. Rosa, PhD a, ⁎∗ Abstract |
Background |
Although different studies associated sleep deprivation (SD) with systemic inflammatory changes, the effect of sleep duration on the pathology of allergic chronic diseases is poorly understood.
Objective |
We sought to evaluate the influence of SD on allergen-induced pulmonary inflammation.
Methods |
Ovalbumin (OVA)–sensitized C57BL/6 mice were exposed to a first set of intranasal OVA challenge under SD or healthy sleep (HS) conditions, followed by a second OVA challenge, 1 week apart. Some groups were subjected to corticosteroid treatment with dexamethasone.
Results |
OVA-sensitized mice with SD had more severe airway inflammation than the allergic group with HS. Analysis of lung parenchyma revealed that the inflammation in allergic mice with SD was marked by an influx of neutrophils (mainly) and eosinophils and secretion of IL-6, TNF-α, and IL-17 in contrast to the eosinophilic inflammation and IL-4 production observed in allergic mice with HS. The same cytokine profile was observed in ex vivo culture of cervical lymph node cells and splenocytes, indicating that in allergic mice SD favors immune responses toward a proinflammatory TH17 profile. This idea is supported by the fact that disruption of IL-17 signaling (IL-17 receptor A−/−) prevented airway neutrophilia in allergic mice with SD. Furthermore, allergic mice with SD became refractory to corticosteroid treatment in contrast to the allergic group with HS.
Conclusion |
Collectively, our data show that sleep quality participates in the progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refractory neutrophilic manifestation.
Le texte complet de cet article est disponible en PDF.Key words : Sleep deprivation, allergic lung inflammation, airway neutrophilia, IL-17, mouse model
Abbreviations used : APC, BALF, CLN, HS, IL-17R, KO, OVA, PBST, PE, PerCP, REM, RT, SD, WT
Plan
| Supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, grants 2014/15061-8, 2012/04692-1). J.S.A., D.A.G.A, and E.R.F received fellowships from CNPq/FAPESP. J.N.O.F received a fellowship from CAPES. |
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| Disclosure of potential conflict of interest: J. O. F. Nunes receives grant support from Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES). D. A. G. Andrade receives grant support from Fundação de Amparo à Pesquisa do Estado de São Paulo–FAPESP. E. R. Fernandes receives grant support from Conselho Nacional de Desenvolvimento Científico e Tecnológico–CNPq. A. C. Keller receives grant support from FAPESP and CNPq. D. S. Rosa receives grant support from Fundação de Amparo à Pesquisa do Estado de São Paulo. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 141 - N° 3
P. 1018 - mars 2018 Retour au numéro
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