Most previous studies have focused on the propagation of epithelial and endothelial injury in ALI/ARDS; the ability of bacteria to colonise host defense mechanisms are not well studied in this pathophysiologic process. Piccin and colleagues [69] examined the hypothesis that mechanical ventilation directly affects respiratory defense mechanisms (the mucociliary system). The authors used different modes of mechanical ventilation in rabbits, and demonstrated that mechanical ventilation using high volume and high pressure led to detrimental changes in the large proximal airway mucociliary system compared with lower tidal volume ventilation. Although a significant decrease in tracheal mucus secretion was noted across all ventilated groups, only animals ventilated with high pressures showed a significant reduction in ciliary beating frequency. The authors speculated that the mucociliary alterations occurred as a result of tissue hypoperfusion caused by mechanical ventilation with high pressures and high airway flows. An editorial [70] pointed out that the relevance of the observation is yet to be investigated in patients under mechanical ventilation. It is nevertheless important to understand the effects of changes in mucociliary clearance in the context of ventilator-induced lung injury that may alter host susceptibility to infections or prolonged intubations due to secretion retention.