Upper airway colLapse and reopening induce inflammation in a sleep apnoea model

¹ Unitat de Biofísica i Bioenginyeria, Facultat de Medicina, Universitat de Barcelona - IDIBAPS, Barcelona, Spain
² Departament Anatomia Patològica, Hospital Clínic, Facultat de Medicina, IDIBAPS, Universitat de Barcelona, Barcelona, Spain
³ Servei Pneumologia, Hospital Clínic, Facultat de Medicina, IDIBAPS, Barcelona, Spain; and CIBER Enfermedades Respiratorias, Spain.
⁴ Unitat de Biofísica i Bioenginyeria, Facultat de Medicina, Universitat de Barcelona - IDIBAPS, Barcelona, Spain; Institut de Bioenginyeria de Catalunya, Barcelona, Spain; and CIBER Enfermedades Respiratorias, Spain.
⁵ Unitat de Biofísica i Bioenginyeria, Facultat de Medicina, Universitat de Barcelona - IDIBAPS, Barcelona, Spain; and CIBER Enfermedades Respiratorias, Spain.

^* To whom correspondence should be addressed. E-mail: rfarre{at}ub.edu.

	Abstract

The upper airway of obstructive sleep apnoea (OSA) patients is subjected to recurrent negative pressure swings promoting its collapse and reopening. The aim of the present work was to ascertain whether this mechanical stress induces upper airway inflammation in a rat model.

The upper airway of Sprague-Dawley rats was subjected to a periodic pattern of recurrent negative (-40 cmH₂O, 1s) and positive (4 cmH₂O, 2s) pressures inducing collapse and reopening for 5 h. Rats instrumented but not subjected to negative pressure swings were used as controls. The gene expression of the proinflammatory biomarkers macrophage inflammatory protein-2 (MIP-2), tumour necrosis factor- (TNF-), interleukin-1 (IL-1) and P-selectin in the soft palate and larynx tissues was assessed by real time PCR (n=8).

A marked over expression of MIP-2, TNF-, IL-1 and P-selectin (40, 24, 47 and 7-fold greater than controls, respectively) was observed in the larynx tissue. Similar results were found in the soft palate tissue: 14, 7, 35 and 11-fold greater than controls, respectively.

Recurrent upper airway collapse and reopening mimicking those experienced by OSA patients triggered an early local inflammatory process. These results could explain the inflammation observed in the upper airway of OSA patients.