Simpson and colleagues observed an increased expression of TLR2, TLR4 and CD14, as well as the proinflammatory cytokines IL-8 and IL-1β in neutrophilic asthma and bronchiectasis patients compared to controls. These groups also had higher airway endotoxin levels than the control group (23) . In another study, there was also an increased pulmonary expression of inflammatory cytokines occurring in the lung during experimental endotoxemia. The cytokine production further contributes to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) (52, 53) . Baumgarten and colleagues showed that LPS induces pro-inflammatory cytokines in the lung via the TLR4/CD14 signaling cascade, suggesting a role of the innate immune response in the pathogenesis of ALI/ARDS (52) .