Molecular and cellular mechanisms of invasion of the intestinal barrier by enteric pathogens. The paradigm of Shigella.

Abstract:

:The pathogenesis of bacillary dysentery can be studied at different levels of integration of the cellular components that constitute the colonic mucosal barrier. We considered the interaction of Shigella flexneri in three experimental systems that provide complementary information and a scheme of events occurring in human colorectal mucosa as Shigella invasion proceeds. Interaction of S. flexneri with individual epithelial cells shows a series of events in which the bacterium, upon contact with the cell surface, releases a set of Ipa proteins (i.e. invasins) through a specialized, activable, type-III secretory apparatus (i.e. Mxi/Spa). Via a complex signaling process, these invasins cause major rearrangements of the subcortical cytoskeletal network which allow bacterial entry by a macropinocytotic event. Then the bacterium lyses its phagocytotic vacuole and initiates intracytoplasmic movement, due to polar assembly of actin filaments caused by a bacterial surface protein, IcsA. This allows very efficient colonization of the host cell cytoplasm and passage to adjacent cells via protrusions which are engulfed by a cadherin-dependent process. However, when invasive Shigella are deposited on the apical side of polarized monolayers of human colonic cells, they appear unable to invade, indicating that bacteria need to reach the subepithelial area to invade the epithelium. In this system, it has been shown that transepithelial signaling caused by apical bacteria induces adherence and transmigration of basal polymorphonuclears (PMN), thus disrupting the monolayer permeability and facilitating bacterial invasion. LPS accounts for a large part of this transepithelial signalization to PMN. Such a process could account for invasion in intestinal crypts. Finally, models of infection, such as the rabbit ligated intestinal loop show that initial bacterial entry occurs essentially via M cells of the follicular associated epithelium. It then causes apoptosis of macrophages located in the follicular dome, inducing release of IL-1 beta which, in turn, initiates inflammation, leading to destabilization of the epithelial structures as modeled above. These data can now be used to understand the mechanisms of mucosal protection against bacillary dysentery.

journal_title

Folia microbiologica

authors

Sansonetti PJ

doi

10.1007/BF02818608

subject

Has Abstract

pub_date

1998-01-01 00:00:00

pages

239-46

issue

3

eissn

0015-5632

issn

1874-9356

journal_volume

43

pub_type

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