Changes in the subcellular localization of TLRs also may play a role in their responsiveness. Dissimilar to plasma membrane localized TLR4 in macrophages, TLR4 has been shown to be localized predominately in the Golgi apparatus in enterocytes (174) , and TLR4 activation in enterocytes has been shown to require intracellular recognition of LPS in the Golgi apparatus and recruitment of IRAK-1 and MyD88 to the Golgi apparatus (195) . Furthermore, colonic HT-29 and colo205 cells express TLR4 predominately in cytoplasmic fractions and are hyporesponsive to LPS in basal states (89) . Intracellular TLR redistribution has been suggested as a mechanism for flagellin tolerance, as prolonged flagellin exposure resulted in redistribution of TLR5 to an intracellular location in T84 colonocytes. Increased cell surface TLR expression also has been suggested as a mechanism of increased TLR sensitivity. Colonic SW480 cells are LPS-responsive and express TLR4 on the cell surface, where LPS internalization is not necessary for TLR4-LPS interaction (89) . Also, increased TLR9 surface expression was noted in response to DNA from pathogenic bacteria in HT-29 colonocytes (196) .