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Mediators Inflamm. 2017;2017:4327237. doi: 10.1155/2017/4327237. Epub 2017 Sep 6.

Alteration of Inflammatory Mediators in the Upper and Lower Airways under Chronic Intermittent Hypoxia: Preliminary Animal Study.

Author information

1
Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Republic of Korea.
2
Department of Pharmacology, Yonsei University College of Medicine, Seoul, Republic of Korea.
3
Department of Chemical and Biomolecular Engineering, Sogang University, Seoul, Republic of Korea.
4
The Research Center for Human Natural Defense System, Yonsei University College of Medicine, Seoul, Republic of Korea.
5
The Airway Mucus Institute, Yonsei University College of Medicine, Seoul, Republic of Korea.

Abstract

PURPOSE:

We hypothesized that CIH may affect the upper airway immune system and aimed to verify whether CIH can induce airway inflammation in a murine obstructive sleep apnea (OSA) model.

METHODS:

C57BL6 male mice were exposed to intermittent hypoxia (CIH group; 5 ~ 21% FiO2, 120 sec cycles, 12 h/d, n = 6) or room air (Sham group, n = 6) for up to 4 weeks in identical chambers. Nasal and lung tissues and lavage fluid were collected and analyzed by multiplex assay. Lung lavage fluid was also utilized for FACS analysis to determine eosinophil count.

RESULTS:

We determined the protein level of 24 different cytokines, chemokines, and inflammatory mediators. Among various cytokines, levels of IL-1α, IL-1β, IL-4, IL-6, and IL-13 were significantly elevated in nose or lung tissue from the CIH group. In addition, MCP-1 and periostin were elevated in nose and lung tissue and lavage fluid from the CIH group.

CONCLUSIONS:

CIH for 4 weeks altered the levels of inflammatory mediators in both the nose and lungs of mouse model. We suggest that the airway immune system may be deteriorated by CIH and allergic inflammation in the upper or lower airway could be worsened by sleep apnea.

PMID:
29038619
PMCID:
PMC5606044
DOI:
10.1155/2017/4327237
[Indexed for MEDLINE]
Free PMC Article

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