Abstract
Tissue invasion by motile cells or organisms is a key step in embryonic development, inflammation, cancer metastasis, and host infection by parasites, fungi, and bacteria (1). In each of these phenomena, tissue invasion is a multifactorial event requiring chemotaxis, motility, adhesion, and tissue degradation. Although each cell or organism has unique properties, any factor identified as being shared in common is of particular importance in helping to define molecular mechanisms of tissue invasion. One of the better characterized factors common to these phenomena is the elaboration of proteinases for tissue degradation. This review will focus on an example of host infection by a multicellular parasite for which proteinase expression is particularly important because of the size of the organism involved and the multiplicity of roles the enzyme can play.
Schistosomes (blood flukes) are trematode parasites that, while infecting a variety of animals, are best known for producing one of the world's major health problems, schistosomiasis (Fig. 1). This disease is endemic throughout much of the tropical world and is estimated to affect over 200 million people (2). The disease itself is produced by a host granulomatous response to eggs laid by adult female worms in the portal venous system. Initiation of infection occurs when an aquatic larval form, the cercaria, invades host skin. Morphologic studies of experimental infections showed that cercariae invade intact skin and tunnel through the epidermis and dermis, eventually entering small blood vessels (Fig. 2). From there, they reach the systemic circulation via the pulmonary vasculature and develop into adults after reaching the portal vein and its tributaries.
Cercariae develop in an intermediate-host fresh-water snail and find their human host by following a thermal gradient (3). Their stimulus for invading the host is lipid on the surface of skin (3).
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