Pulmonary inflammatory diseases represent a broad spectrum of conditions that include allergic asthma, acute lung injury and acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD), and infectious pneumonia (96 has a recent review). Although these diseases traditionally have been considered to reflect the combined effects of activation of the adaptive immune system with the release of antibodies and mobilization of host immune cells, recent evidence has demonstrated an important role for the TLR family members of the innate immune system in their pathogenesis. And, in parallel with the mechanisms leading to the development of mucosal inflammation in the intestine, an emerging body of literature now provides evidence that epithelial TLR signaling plays a central role (15) . Previous authors have shown that the pulmonary epithelium expresses a variety of TLRs (see Table 3 ), suggesting their role in the pathogenesis of pulmonary inflammation. In support of a role for TLR signaling in the pulmonary epithelium in the development of pulmonary inflammation, Noulin et al. have demonstrated that TLR4 and MyD88dependent signaling are required for the bronchoconstriction, cytokine response, protein leak, and neutrophil recruitment observed in response to inhaled endotoxin (28) . Furthermore, using MyD88-/bone marrow chimeras, Noulin et al. demonstrated that both resident and hematopoietic cells are necessary for the mucosal inflammatory response to inhaled endotoxin (28). Hajjar et al. demonstrated that MyD88-deficient mice transplanted with bone marrow from MyD88-expressing mice showed reduced chemokine production compared with MyD88 expressing mice that were transplanted with MyD88-expressing bone marrow in a model of experimental Pseudomonas aerogeninosa pneumonia, indicating a requirement for resident pulmonary parenchymal cells in the response to experimental pneumonia. The local pulmonary cytokine response was predominately dependent on competent MyD88 signaling in bone-marrow derived cells, suggesting that collaboration between local parenchymal cells, including epithelial cells, and bone-marrow derived cells is required (29) . In a model of bacterial pneumonia that utilizes inhaled LPS, the uptake of LPS was observed in bronchial epithelial cells and was associated with increased TLR2 and TLR4 expression in the bronchial epithelium (97) . Similarly, in an equine model of recurrent airway obstruction associated with inhaled endotoxin-rich stable dust, increased epithelial expression of TLR4 was observed and was associated with increased IL-8 expression by the airway epithelium (98) . Taken together, these reports provide supportive evidence for an important role for epithelial TLR signaling in the pathogenesis of mucosal inflammation in the pulmonary system.