Sleep deprivation predisposes allergic mice to develop neutrophilic lung inflammation.

Sleep deprivation predisposes allergic mice to develop neutrophilic lung inflammation.:

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Sleep deprivation predisposes allergic mice to develop neutrophilic lung inflammation.

J Allergy Clin Immunol. 2017 Jul 18;:

Authors: de Oliveira Filho JN, Apostolico JS, Andrade DAG, Silva FRD, Fernandes ER, Andersen ML, Keller AC, Rosa DS

Abstract

BACKGROUND: Although different studies associated sleep deprivation with systemic inflammatory changes, the effect of sleep duration on the pathology of allergic chronic diseases is poorly understood.

OBJECTIVE: To evaluate the influence of sleep deprivation on allergen-induced pulmonary inflammation.

METHODS: Ovalbumin (OVA)-sensitized C57BL/6 mice were exposed to a first set of intranasal OVA challenge under sleep deprivation (SD) or healthy sleep (HS) conditions followed by a second OVA challenge, one week apart. Some groups were subjected to corticoid treatment with dexamethasone.

RESULTS: OVA-sensitized SD mice developed a more severe airway inflammation than the HS allergic group. Analysis of lung parenchyma revealed that the inflammation in SD allergic mice 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 HS allergic mice. The same cytokine profile was observed in ex vivo culture of cervical lymph nodes cells and splenocytes, indicating that in allergic mice SD favors immune responses towards a pro-inflammatory Th17 profile. This idea is supported by the fact that disruption of IL-17 signaling (IL-17RA(-/-)) prevented airway neutrophilia in allergic SD mice. Furthermore, SD allergic mice became refractory to corticoid treatment, in contrast to HS allergic group.

CONCLUSION: Collectively, our data show that sleep quality participates in the progression of allergen-induced eosinophilic lung inflammation to corticoid refractory neutrophilic manifestation.

PMID: 28732645 [PubMed - as supplied by publisher]

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