Dr. Murai Éva szerk.: Parasitologia Hungarica 22. (Budapest, 1989)
HOW CAN IMMUNITY INTERFERE WITH WORM PHYSIOLOGY? From this overview it is seen that despite considerable effort in attempting to specify the effector components of the potential antl-parasite armaments of the host no direct causal connection between individual elements of host reaction and worm expulsion from the gastrointestinal tract h as been convincingly established. What is clearly established, is that helminth infection triggers a complex interplay between antigens, antibodies, host cells, and mediators leading to local inflammatory response. The structural and functional changes associated with the local intestinal anaphylactic reaction are summarized in Fig. 4 (WAKELIN 1986). These pathological changes, once developed, create an environment Inhospitable for attachment and feeding of the intestinal nematodes, and the ensuing acute metabolic crisis of the worms renders them vulnerable by the nonspecific mechanism of expulsion. It has been shown that adult intestinal nematodes are not killed, but reversibly damaged when expelled from the bowel , and it is presumed that the damage is essentially a transient metabolic depression (MOQBEL et al. 1980; KENNEDY and BRUCE 1981; KASSAI et al. 1987). A detailed analysis ot the nature of metabolic depression seen in immune damaged CELLULAR AND STRUCTURAL CHANGES Altered epithelial cell kinetics Villous atrophy, crypt hyperplasia Infiltration by eosinophils, macrophages, neutrophils Mastocytosis Increased goblet cells Increased plasma cells Increased intraepithelial lymphocytes Membrane changes in epithelial cells Dedifferentiation Mucosal oedema PHYSIOLOGICAL CHANGES Increased secretion of mucus Increased vascular and epithelial permeability Increased net fluid secretion across mucosa Fluid accumulation in lumen Increased motility Decreased transit time MEDIATOR CHANGES Increased levels of Ig in lumen Increased levels of myeloperoxidase and phospholipase Increased levels of histamine, serotonin, leukotrienes, prostaglandins Fig. 4 Infection induced changes in intestinal structure and function (Wakelln, 19861
