Several groups have shown that airway epithelial cells (AEC) express TLRs and secrete cytokines in response to TLR activation. AECs have been shown to express TLR2 and TLR4 and release IL-8 in response to Streptococcus pneumoniae, lipoteichoic acid, and lipopolysaccharide (99, 100) . Furthermore, TLR9 activation in bronchial epithelial cells has been shown to potentiate IL-8 release from bronchial epithelial cells (101) . Although it has been shown that multiple TLRs may signal in the airway epithelium (15) , microarray analysis of the lung has revealed that TLR4 signaling accounts for 74% of the pulmonary response to experimental Klebsiella pneumoniae pneumonia by comparing the pulmonary response in wildtype mice to C3H/HeJ TLR4 mutant mice. The particular TLR4-dependent responses included genes that are involved in cytokine and chemokine induction, neutrophil activation and recruitment, growth factor receptors, and TLR adaptor molecules (102) .