Lung epithelial and alveolar macrophage-like cell interactions significantly modify innate responses to bacterial endotoxin with the involvement of direct cellular contacts, TNF-α, ICAM1 and MCP-1

Together, these findings identify cellular contacts and a TNF-a-ICAM-1-MCP-1 axis-supported by epithelial-derived LBP-as key drivers of innate immune synergy between lung alveolar macrophages and epithelial cells. Our results establish the MPI-MLE-12 co-culture as a tractable model for dissecting pulmonary innate immune mechanisms.