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American Journal of Pathology, Vol 87, 105-123, Copyright © 1977 by American Society for Investigative Pathology

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A lung model of schistosome immunity in mice

F von Lichtenberg, A Sher and S McIntyre

When mice are challenged intravenously with schistosomula of Schistosoma mansoni, host cell reaction and parasite attrition proceed entirely in the lung, where these events can be followed by quantitative histology and worm recovery. In nonimmune animals the destruction of schistosomula in the lungs proceeds gradually, resulting in the elimination of about 80% of the challenge organisms after 6 days. Cell reaction begins promptly, as evidenced by the appearance of neutrophilic foci around many of the lung schistosomula within 30 minutes after injection, and results in increasing numbers of damaged organisms and residual inflammatory foci 24 hours and 6 days later, respectively. In contrast, when schistosomula are injected into mice immune by virtue of an established S. mansoni infection, parasite destruction is augmented and accelerated, a process already evident by 24 hours. By the sixth day, 98% of the challenge organisms have been eliminated, a substantially greater reduction in parasite survival than that occurring in the normal host. This increased attrition of schistosomula is also reflected in the decreased numbers of parasites recovered from minced lung tissue of immune mice 6 days after challenge. Immune cellular inflammatory reactions to schistosomula are, likewise, greatly intensified and can be readily distinguished from those of normal mice by the proportions of parasites involved and by the large numbers of eosinophils surrounding them. In some instances, degranulation of eosinophils onto the parasite tegument is observed. Schistosomula cultured for 24 or 44 hours in a medium containing mouse red blood cells elicit significantly less cellular reaction and show greater survival in the lungs of immune animals than do freshly derived schistosomula. It would therefore appear that the susceptibility of maturing schistosomes to immune cellular attack is limited to the first day or two after their metamorphosis from cercariae. These observations form the framework of a new in vivo model for analyzing the dynamics of the cellular and humoral processes involved in the immune destruction of a metazoan parasite. The model also lends itself to studies of the immunologic interrelationships between innate and acquired resistance to infection with schistosomes, as well as the mechanisms by which these parasites evade the host immune response.

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