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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital parasitic infections may not lead to any overt clinical effects but could modulate the foetal future immune response to the same parasite depending on whether sensitization or tolerance has occurred in utero. In this study, pregnant female mice were infected with Toxocara canis eggs at different gestational age, then the offspring were next challenged with Toxocara eggs 6 weeks after birth and their immune response was assessed by estimation of the eosinophilic count and serum IgE concentration. The Total larval count (TLC), brain parasitism (BP) and reduction % in (TLC) were used as criteria for the course of infection. It was found that exposure to infection during pregnancy whether early or late led not only to transmission of larvae to the foetus but also to modulation of its immune response and course of infection when next encountered the parasite after birth. The offspring when compared to control from non-infected mothers were hyporesponsive when infection occurred early during pregnancy and they showed high immune responsiveness when infection was induced late in pregnancy. The potential clinical application of these findings was suggested. It is now an established fact that immunocompetence in the mammalian foetus including humans develops very early in utero. Therefore, the foetus is capable of showing some forms of activity against invasion by maternal pathogenic organisms or their antigens (Loke, 1978). Moreover, the early contact with parasitic antigens may affect the foetus future immune response when it next encounters similar organisms after birth. Palmer (1978) reported a rapid secondary immune response in the offspring of Plasmodium berghei infected female rats when challenged with the parasite and compared to control groups from non-infected mothers. An apposite response was reported by Hang et al. (1974) who noticed that massive infection of pregnant mice with Schistosoma mansoni cercariae resulted in offspring hyporesponsive to subsequent challenge assessed by the diameter of the egg granulomas. Considering that toxocariasis is a frequent and potentially serious disease affecting primarily young children, also congenital toxocariasis was well documented since the original studies of Fulleborn (1921), this study was designed to reveal the extent to which the foetus future immune response can be modulated by maternal toxocariasis in experimental animals. The estimation of the immune response included IgE level (antibody mediated mechanism) and the absolute eosinophils count (a manifestation of cell mediated immune response) since eosinophil/IgE/mast cell axis represents a specialized immune mechanism that may contribute directly to parasite damage in toxocariasis (Knight, 1982). Also, (TLC), (B.P) and reduction % in (TLC) were used as criteria for the course of infection.
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PMID:Experimental congenital toxocariasis: effect on foetal future immune response. 891 35

It is well known that eosinophilia is a key pathogenetic component of toxocariasis. The objective of the present study was to determine if there is an association between peritoneal and blood eosinophil influx, mast cell hyperplasia and leukotriene B(4) (LTB(4)) production after Toxocara canis infection. Oral inoculation of 56-day-old Wistar rats (N = 5-7 per group) with 1000 embryonated eggs containing third-stage (L3) T. canis larvae led to a robust accumulation of total leukocytes in blood beginning on day 3 and peaking on day 18, mainly characterized by eosinophils and accompanied by higher serum LTB(4) levels. At that time, we also noted increased eosinophil numbers in the peritoneal cavity. In addition, we observed increased peritoneal mast cell number in the peritoneal cavity, which correlated with the time course of eosinophilia during toxocariasis. We also demonstrated that mast cell hyperplasia in the intestines and lungs began soon after the T. canis larvae migrated to these compartments, reaching maximal levels on day 24, which correlated with the complete elimination of the parasite. Therefore, mast cells appear to be involved in peritoneal and blood eosinophil infiltration through an LTB(4)-dependent mechanism following T. canis infection in rats. Our data also demonstrate a tight association between larval migratory stages and intestinal and pulmonary mast cell hyperplasia in the toxocariasis model.
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PMID:Evidence for eosinophil recruitment, leukotriene B4 production and mast cell hyperplasia following Toxocara canis infection in rats. 2148 43