EspA makes filamentous appendages outside the bacterium and may be part of the translocation machinery involved in delivering other virulence proteins (11). The translocation of these proteins is essential for activating a number of signal transduction pathways (7), although their precise role in pathogenesis is not well defined. The expression of these proteins is maximal at the host body temperature (9) and at conditions similar to those found in the gastrointestinal tract (10), which implies that they may be involved in virulence. The second stage of EPEC pathogenesis involves the secretion of bacterial proteins, some into the host cell, including EspA, EspB, and EspD ( 7, 8). coli attaching and effacing that encodes intimin), and tir (translocated intimin receptor) genes (6). BFP mediate bacterial-bacterial interactions in a human intestinal organ culture model (3).Īll the genes necessary for the formation of A/E lesions by EPEC are contained within a 35-kbp pathogenicity island termed the locus of enterocyte effacement (LEE) ( Figure 1B) ( 4, 5).
While not essential for forming the characteristic A/E lesions, initial adherence helps bring the bacteria in close contact with the host cell. Initial adherence to cultured epithelial cells is mediated by the formation of type IV fimbriae known as bundle forming pili (BFP) (2). The interactions between EPEC and host cells have been divided into three stages. Bacterial Factors Involved in EPEC-Induced A/E Lesion Formation
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