A study by Togbe et al. of whether TLR gene dosage contributes to infection has demonstrated that overexpression of TLR4 augmented an LPS-induced bronchoconstrictive effect, as well as TNF-α and CXC chemokine ligand 1 (keratinocyte-derived chemokine) production (55) . The study further showed that PMN recruitment, microvascular and alveolar epithelial injury with protein leak in the airways, and damage of the lung microarchitecture were dependent on TLR4 gene dose. Therefore, the TLR4 expression level determines the extent of acute pulmonary response to inhaled LPS, and TLR4 may thus be a valuable target for immunointervention in acute lung inflammation as a result of infection.