Regulation of epithelial TLR expression has been suggested as a mechanism for the regulation of epithelial cell responsiveness in the setting of commensal bacterial exposure and during disease states. For instance, low expression of TLR4, as has been observed in colonic biopsies from humans (75) , has been suggested as a mechanism for colonocyte LPS hyporesponsiveness. Similar findings of low TLR4 expression have been observed in colonocyte cell lines (HT-29, SW480, colo205) and increased TLR4 expression after IFN-γ or TNF-α priming, as may occur during inflammatory states, has been shown to enable LPS responsiveness (88) . Similarly, low expression of TLR2 has been implicated in bronchial epithelial cell hyporesponsiveness to Gram-positive bacteria (15) .