Dr. Murai Éva szerk.: Parasitologia Hungarica 22. (Budapest, 1989)

mediators per se possess a direct worm damaging capacity (ROTHWELL, PRICHARD and LOVE 1974). Heparin can enhance vascularisation at sites of inflammation. Serine protein ases - as it has already been mentioned - contribute to the generation of the inflammatory reaction. A direct worm damaging effect of prostaglandins of the E class was proposed (KELLY and DINEEN. 1976; RICHARDS et al. 1977). KASSAI et al. (1980), however, could not verify any direct adverse effect of prostaglandins on adult worms neither under in vitro nor in vivo conditions. Leukotrienes,

formerly defined as slow reacting substance of anaphylaxis, are arachidonic acid metabolites known as chemotactic mediators and modulators of histamine release, bronchoconstriction and vasodilatation. Whether they have a direct helminthotoxic potential, is unknown. However, they probably contribute to the immediate type hypersensitivity reaction of the intestine and to anamnestic mucus production, as suggested by results of MOQBEL et al. (1987). Several mast cell functions have already been mentioned in relation to the activities of mast cell mediators. It is now expedient to summarize the range of mast cell functions (Fig. 3). It must be noted that mast cell characteristics were largely determined using peritoneal mast cells. Whether the variable functions of these subsets of mast cells occur also in MMCs is likely but not yet proven. Ad c) Mast cell mediator antagonists have also been used to investigate the contribution of these cells to the protective response to Intestinal helminths. The results obtained are controversial. Earlier studies suggested that treatment with promethazine (histamine antagonist), Cimetidin (histamine type 2 H2/receptor antagonist), and inhibitors of prostaglandin synthesis might delay the expulsion of intestinal nematodes. In recent studies of BUIJS et al (1987) and P

ARMENTIER et al. (1987) by blocking serotonin receptors with two serotonin antagonists, methysergide and ketanserine, it was possible to suppress the inflammatory response in the gut of mice infected with T. spiralis

, as expressed by marked depression on numbers of MMC, eosinophilic granulocytes and goblet cells in the parasitized jejunum. At the same time tha ability of the mice to expel adult worms was not affected, suggesting that the role played by MMCs In worm expulsion is only minor and dispensable. Ad d

) This observation gained further support from investigations carried out with mouse strain W/W

v

which is known to be genetically mast cell deficient

. In initial studies reported by UBER et al, (1980) it was found that the time course of immune expulsion of N. brasiliensls was similar in mast cell deficient and normal mice. In subsequent studies using the same W/W

v strain of mice, expulsion of both N. brasiliensls (MITCHELL et al. 1983; CROWLE and REED 1983) and T. spiralis (HA et al. 1983) was somewhat delayed but not inhibited. OKU et al. (1984) and NAWA et al. (1985) reported a more significant delay In the rejection of N. brasiliensls as well as T. spiralis and Strongyloides ratti, respectively, in these mice. Eventually, these animals do possess the capacity of expelling intestinal nematodes. These varying results appear to reflect that the supposedly mast cell deficient hosts may contain a low number of functional mast cells which are perhaps undetectable by classical histochemistry. Indeed, In studies reported by ALIZA DE H and WAKELIN (1982), ALIZADEH and MURRELL (1984) and WAKELIN (1985) evidence was produced to show that also W/W

v mice develop MMC hyperplasia In response to T. spiralis infection although it is much diminished and delayed. It has therefore been suggested to define the W/W

v strain of mice as genetically slow responder rather than "mast cell deficient"

. On the other hand, It was also pointed out by WAKELIN et al. (1985) that low MMC responders were also slow responders with regard to worm expulsion. Summing up briefly, the actual role of mast cells in the protection of hosts against intestinal helminths remains to be elucidated.