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

¹ Unitat de Biofísica i Bioenginyeria, Facultat de Medicina, Universitat de Barcelona, Institut d’Investigacions Biomèdiques Augustí Pi i Sunyer (IDIBAPS), ² Dept Anatomia Patològica, Hospital Clínic, ³ Servei Pneumologia, Hospital Clínic, ⁵ Institut de Bioenginyeria de Catalunya, Barcelona, and ⁴ Centro Investigación Biomédica en Red de Enfermedades Respiratorias, Bunyola, Spain.

CORRESPONDENCE: R. Farré, Unitat de Biofísica i Bioenginyeria, Facultat Medicina, Casanova 143, 08036 Barcelona, Spain. Fax: 34 934035278. E-mail: rfarre{at}ub.edu

Keywords: Airway collapse, airway reopening, inflammation, negative pressure, obstructive sleep apnoea, upper airway

Received: November 30, 2007
Accepted April 16, 2008

The upper airway of obstructive sleep apnoea patients is subjected to recurrent negative pressure swings promoting its collapse and reopening. The aim of the present study 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, 1 s) and positive (4 cmH₂O, 2 s) pressures inducing collapse and reopening for 5 h. Rats that were instrumented but not subjected to negative pressure swings were used as controls. The gene expression of the pro-inflammatory biomarkers macrophage inflammatory protein (MIP)-2, tumour necrosis factor (TNF)-, interleukin (IL)-1β and P-selectin in the soft palate and larynx tissues was assessed by real-time PCR.

A marked overexpression of MIP-2, TNF-, IL-1β 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 obstructive sleep apnoea patients triggered an early local inflammatory process. These results could explain the inflammation observed in the upper airway of obstructive sleep apnoea patients.