Evasive strategies of the organism

L. monocytogenes can invade and multiply within mononuclear phagocytes, hepatocytes and epithelial cells (Figure 2). It produces a series of virulence factors that enable it to invade cells, multiply intracellu-larly, and directly invade adjacent cells. This results in foci of infection that can be readily demonstrated by histopathology. These virulence determinants are positively regulated in a coordinated manner by the product of the prfA gene. A surface protein, called internalin, facilitates adherence and invasion of mammalian cells via interaction with E-cadherin (Figure 2, step A). Another L. monocytogenes protein (p60), which can be found on the bacterial surface or secreted into the culture medium, also affects interaction with mammalian cells. Once it invades a mammalian cell, L. monocytogenes escapes from the

membrane-bound phagosome by the action of its hemolysin and two phospholipases C, one of which has broad activity and the other of which is phos-phatidylinositol specific (step B). The listeriae then multiply freely within the cytoplasm (step C) and express a surface protein, called actA, that serves as a nucleation point for the attachment of actin filaments (step D). This occurs in a unidirectional manner such that new actin subunits are continually placed on the surface of the bacterium, resulting in formation of a long (up to 40 pm) actin tail. These actin tails can propel L. monocytogenes at speeds of up to 1 pm s ', driving some of them through the cytoplasmic membrane of the original cell and into the cytoplasm of an adjacent cell (step E). The listeriae then escape from the double membrane-bound phagosome in which they find themselves (step F), and repeat the replication cycle (step G). Cellular and humoral immune responses to the hemolysin, internalin, and actA have been demonstrated. Which of these responses is most important for restricting the multiplication of the organism is not clear.

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