Mucosal mast cell-derived chondroitin sulphate levels in and worm expulsion from FcRgamma-knockout mice following oral challenge with Strongyloides venezuelensis

Mucosal mast cell-derived chondroitin sulphates (sulphated proteoglycans) were assayed in gut washings and homogenate of FcRgamma-knockout (KO) and wild-type (WT) C57BL/6 mice challenged with Strongyloides venezuelensis in order to assess their possible role in secondary immunity against enteric nematodes. Groups of immune KO and WT mice were challenged by oral gavage with 300 infective larvae (L3). Establishment of infection was assessed by daily faecal analysis to determine the number of eggs per gram of faeces (EPG) and by adult worm recovery on days 5 and 13 post challenge. Mucosal mast cell (MMC) counts were done on days 5 and 13 post challenge while MMC-derived chondroitin sulphates in gut washings (days 1 and 5) and homogenate (day 8) were assayed by high performance liquid chromatography (HPLC). Results showed that patent infection occurred in challenged KO but not WT mice despite significantly higher mastocytosis in jejunal sections of KO than WT mice (p<0.001). Similarly but against prediction, significantly higher concentration of MMC-derived chondroitin sulphates was observed in gut homogenate of KO than WT mice (p<0.05). In contrast, significantly higher concentration of chondroitin sulphates was observed in gut washings of WT than KO mice (p<0.05). These results suggest that MMC in KO mice failed to release sufficient amount of sulphated proteoglycans into the gut lumen as did the WT mice, which may have been part of the hostile environment that prevented the establishment in and eventual expulsion of adult S. venezuelensis from the gut of WT mice following challenge.

Lack of significant association between rosette formation and parasitized erythrocyte adherence to purified CD36.

The ability of Plasmodium falciparum infected erythrocytes from 162 Thai patients with uncomplicated malaria, 82 patients with severe malaria and 19 patients with cerebral malaria to form rosettes in vitro was studied. Of 263 isolates, 62 were evaluated for their adherence to different target molecules. We found that wide variation occurred in isolates from all groups in the level of rosette formation and adherence to CD36, intracellular adhesion molecule-1, thrombospondin and chondroitin sulfate A. No statistically significant correlation between the magnitude of rosette formation and disease severity was found (p > 0.05). In addition, our results from the use of purified CD36 as an adherence receptor showed no association between the degree rosetting and level of cytoadherence (p > 0.05, r = -0.04). Our data provide evidence that rosette formation and cytoadherence involve different molecular mechanisms and both phenomena can occur in all manifestations of the disease.