Shigella flexneri enters human colonic Caco-2 epithelial cells through the basolateral pole

Abstract

The commonly accepted view that enteroinvasive bacteria enter cells of the intestinal epithelial lining through the apical surface can be challenged in the case of shigellosis. This study is based on in vitro experiments that showed that the invasion of human colonic Caco-2 cells by Shigella flexneri occurred through the basolateral pole of these cells. In these experiments, the few bacteria that interacted with the apical surface either bound to microvilli of the cell dome without causing detectable alteration or bound at the level of intercellular junctions at which they demonstrated a limited capacity for paracellular invasion, which permitted subsequent entry through the lateral domain of the cells. Treatment of Caco-2 cell monolayers with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA), which disrupts intercellular junctions, greatly enhanced the rate of cell infection. These observations suggest a physiopathological paradox that may have important consequences for the understanding of the process of colonic invasion in vivo during shigellosis.

Binding of Clostridium difficile to Caco-2 epithelial cell line and to extracellular matrix proteins

“…Moreover, microscopic observations of noncon£uent monolayers revealed that bacteria adhered mainly to the outer edge of peripheral cells of the islets. This pattern of adherence resembled that of some enteroinvasive bacteria that enter through the basolateral surface of di¡erentiated and nondi¡erentiated polarized Caco-2 cells [4,5].…”

Cooperation ofSalmonellapathogenicity islands 1 and 4 is required to breach epithelial barriers

“…and S. enterica. Shigella cannot invade epithelia from the apical side and the current model proposes that Shigella has to be transcytosed through M cells to be able to invade epithelial cells from the basolateral side by a mechanism that is similar to the SPI1-mediated invasion of Salmonella (Mounier et al, 1992;Nhieu and Sansonetti, 1999). As the invasion of M cells has also been reported for Salmonella (Jones et al, 1994), basolateral invasion of epithelial cells might also be deployed by Salmonella.…”

How intestinal epithelial cell differentiation inhibits the cell-entry of Yersinia pseudotuberculosis in colon carcinoma Caco-2 cell line in culture

“…Our results showing in vitro that asp, integrin, the receptor for Yersinia invasin, which plays a primary role in the initiation of infection 1391, does not appear accessible for cell infection after the Caco-2 cells commence their differentiation or are fully differentiated, explain why Yersinia species cannot invade differentiated intestinal epithelial cells in vivo. Other enteroinvasive bacteria, such as Lisreria monocytogenes [ 12, 131 and Shigella j k x n e r i [34], can promote infection of undifferentiated Caco-2 cells and cannot enter the apical side of polarized differentiated Caco-2 cells. For S. j k x n e r i , the cell adhesion molecule L-CAM is required for cell-to-cell spread [34, 451. In contrast to s. ,flexnevi and I: pseudotuberculosis, we have observed that neither aJ3, integrins nor E-cadherin is involved in infection of undifferentiated Caco-2 cells by L. monocytogenes (M.-H. Coconnier, personal communication).…”