Furthermore, this activation process is associated with an increased intracellular content of the pro-inflammatory mediators Tumor necrosis factor (TNF) α and interleukin (IL)-8 and, a decrease of the anti- inflammatory cytokine IL-10 [8], in accord with the observation that in OSA patients repetitive airway obstructions causing intermittent hypoxia induces activation of nuclear factor-κB (NF-kB) and upregulation of pro-inflammatory genes [9]. Here, TNF is linked to Airway obstruction.