TLR4 and acute respiratory distress syndrome: Although GPCRs (β2-AR) protect the endothelial barrier and cell structure and function against damage from LPS-induced hyperpermeability at the HPMEC surface [12], Toll-like receptors (TLRs), especially TLR4 which is an essential contributor to inflammation in ALI/ARDS, are the main effectors of the LPS-induced inflammatory response.