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Dietary Lectins and the Possible Mechanisms Whereby They Induce Intestinal Injury

Diarrhea of infancy and early childhood has many causes, including viral and bacterial infection. In some of these conditions the intestine may demonstrate few if any histological changes (e.g., cholera) or may show profound alterations (e.g., Salmonella, reovirus, etc.). One of the more common reactions of the intestine to various insults is the development of the "flat villus" pattern (Table 1). In general, this type of reaction is characterized by increased crypt mitotic activity and some tendency for "less mature" villus cells. The presence of an increased density of immature villus cells facing the intestinal lumen may have two important pathophysiological effects that may contribute to a slower recovery or to the establishment of a chronic condition. One effect is the likelihood that the less mature villus cells would have less efficient absorbing and brush border hydrolytic activities; the second, acquired lactose intolerance, is used as an explanation for an increased sensitivity to milk. This second effect presumably reflects the fact that the less mature villus cell would have a different plasma membrane structure (1), particularly in regard to the composition of the oligosaccharide chains of the constituent glycoproteins and glycolipids. These structural alterations in cell surface carbohydrate may make the cell more susceptible to the effects of dietary lectins, substances present in a normal diet that bind glycoproteins. Nachbar and Oppenheim (la) have recently enumerated the dietary lectins uncovered to date (Table 2). In this chapter we discuss the evidence for lectin-induced intestinal injury and four interrelated mechanisms that may explain it.