Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The intestinal mast cell response and lymphoblast activity, as measured by the incorporation of 3H-thymidine into mesenteric lymph node cells (MLN) of WBB6F1-w/wv(w/wv) mice, their normal congenic littermates (+/+) and C57BL/6J mice, were compared after infection with Trichinella spiralis. Marked and similar blast cell activity and an increase in number of cells were observed in the MLN of infected w/wv and C57BL/6J mice 7 and 15 days P.I. In contrast to C57BL/6J mice, primary T. spiralis intestinal infections were prolonged in w/wv mice and more muscle larvae were recovered from w/wv mice 29 days post-infection. In C57BL/6J mice mucosal mast cell (MMC) numbers increased on day 7 P.I. whereas in w/wv mice these cells did not increase significantly until day 15 post-infection, reaching a peak on day 22. In w/wv mice, the response to secondary infection as determined by an accelerated expulsion of adult worms did not occur until day 11 postchallenge whereas in +/+ and C57BL/6J mice worm expulsion was nearly complete at that time. In both primary and secondary infections, the MMC numbers in w/wv mice were significantly lower than in C57BL/6J or +/+ mice. The results suggest that prolongation of T. spiralis infection in w/wv mice is associated with delayed appearance of mast cells in the intestinal mucosa which may reflect slow generation of the intestinal inflammatory response.
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PMID:The intestinal mast cell response to Trichinella spiralis infection in mast cell-deficient w/wv mice. 651 40

Various aspects of the allergic reactivity of Amerindians in the Venezuelan sector of the Amazon basin were examined. The frequency of positivity in immediate hypersensitivity skin tests with extracts of common local environmental allergens was found to be extremely low (6.7%). As sera from significantly higher proportions of the study group contained specific IgE antibody against the test allergens, and their histamine-induced skin responses were normal, these results support previous suggestions of an inhibited expression of allergic reactivity in such populations. Indeed, the intense helminthic infections detected, and the extremely high total serum IgE levels measured (geometric mean 13,088 IU/ml) indicate the possible occurrence of mast cell saturation by parasite-induced IgE. However, despite a similar lack of agreement between the in vivo and in vitro tests for allergic reactivity against Ascaris lumbricoides in these subjects (43.5 and 97.9% positive, respectively), their extremely high responsiveness to the helminth allergens presents a marked contrast to that against the other environmental materials. Factors other than helminthiasis (e.g. racial, cultural, nutritional) might, therefore, also modulate the expression of allergic reactivity in such populations.
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PMID:Allergic reactivity and helminthic infection in Amerindians of the Amazon Basin. 664 8

The changes in numbers of 6 cell populations in the intestine of mice at various intervals after primary and challenge infections with Strongyloides ratti have been quantified. The number of lamina propria mast cells increased 8 days after primary infection and reached a peak at 12 days. After secondary infection, there was a transient fall in mast cell numbers followed by a slow increase. Globule leucocytes showed a similar trend early in the primary infection and had reached normal levels after 28 days. After challenge infection, there was an early and rapid increase in their numbers. Granular intraepithelial lymphocytes did not alter significantly during the first 14 days, but were significantly greater 28 days after primary infection; they did not vary significantly after challenge infection. However, numbers of non-granular intraepithelial lymphocytes increased 10 days after infection, were elevated prior to the secondary infection at 28 days, then declined in numbers nearly 2 weeks after challenge infection. Goblet cells increased significantly 12 days after primary infection then declined rapidly. After challenge infection, there was an accelerated increase in numbers. Eosinophil numbers increased 4 days after infection, reached a peak at 12 days and then declined. After challenge infection, there was an augmented and accelerated increase in eosinophil numbers followed by rapid decline. The role of the various cells types in host defences against worms or in containment of the inflammatory responses evoked by these parasites are discussed.
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PMID:Kinetics of intestinal lamina propria mast cells, globule leucocytes, intraepithelial lymphocytes, goblet cells and eosinophils in murine strongyloidiasis. 673 88

Nippostrongylus brasiliensis infection of rats and mice is a model for studying immunity at mucosal surfaces. Adult worms are spontaneously expelled from the intestine at the end of the second week of infection. Expulsion from the jejunum requires the presence of immune T lymphocytes and IgG antibodies. Mucosal mast cells (MMCs) are a prominent part of the jejunal inflammatory response. They are derived from a hematopoietic stem cell, possibly the same precursor as basophils. Their differentiation is not absolutely T dependent but their accumulation at the site of infection is. The possible involvement of IgE antibodies and intestinal MMCs through a "leak lesion" is still uncertain. Increased mucus secretion from epithelial goblet cells is also a prominent feature of the inflammatory reaction at the site of infection. Goblet cell numbers increase two to four times at the onset of worm expulsion; this increase is regulated by T lymphocytes and possibly immune serum. The mechanism of mucus secretion in these infections is not clear; it may be a response to mast cell mediators. Together with antiworm antibodies, intestinal mucus may trap worms and prevent them from surviving in the intervillous spaces of the jejunum. Thus, expulsion of this intestinal parasite may occur through a nonspecific process that is induced by specific immune mechanisms.
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PMID:Immunity to intestinal parasites: role of mast cells and goblet cells. 683 97

Anti-thymocyte-serum (ATS) treated Wistar rats infected with 100 cysticercoids of the rat intestinal cestode Hymenolepis diminuta showed a delayed destrobilation and expulsion of the worms compared with saline-treated infected rats. This result strengthens previous evidence of an immunological nature of the destrobilation and expulsion in lumen-dwelling cestodes--even in their most susceptible hosts. The migration of the worms in the small intestine during the first 20 days of a primary 100-worm infection is described and the anterior migration of the destrobilated worms to the first 10% of the pylorus is emphasized and compared with similar migrations of the nematode Nippostrongylus brasiliensis in the rat. No serum antibodies were detected using passive cutaneous anaphylaxis and the indirect immunofluorescence test, although the thymus-independent areas of the mesenteric lymph nodes showed an increase in pyroninophilic cells. In the small intestine, no response to the tapeworm infection could be detected in pyroninophilic cells and globule leucocytes, but mast cell and eosinophilic cell numbers were increased in the saline-treated infected rats. Although the host responses to H. diminuta are shown to be thymus-dependent, the possibility of thymus-independent activity in the host reactions cannot be ruled out.
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PMID:Immunological and histopathological reactions of the rat against the tapeworm Hymenolepis diminuta and the effects of anti-thymocyte serum. 697 26

An investigation of the pathologic events occurring during experimental Strongyloides ratti infection in rats was done. The chronologic sequence of the cellular responses to the infecting larvae as they migrated through the skin and lungs was determined. Larvae penetrate the skin very quickly, eliciting considerable mast cell degranulation within the first few minutes, a modest neutrophil response within the first few hours, and an occasional mononuclear response within the first 2 days. The larval passage in the lungs appears to cause little damage except for microhemorrhages and an occasional microabscess. In the intestine S ratti adult worms lie in the cryptae without penetrating mucosa, and except for an increase in the number of mast cells at the time of expulsion (Days 20--25), there is no detectable cellular response. Differences from the human disease are discussed.
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PMID:The histopathology of experimental strongyloidiasis. 736 57

The duration of primary infections with T. spiralis was dose-dependent with greater proportional loss of worms from heavily infected hamsters and longer persistence of worms in syngeneic DSN hamsters carrying initially low intensity infections. Intestinal worms were lost more rapidly from challenged immunized animals with over 80% loss of established worms by day 6 post infection, but survival of residual worms for a further 2 weeks. Hamsters carrying initially more than 140 intestinal worms began to lose weight during the second week indicating severe pathology at this stage of infection. Mucosal mast cell numbers increased from 50 cells/20 villus crypt units in uninfected animals to a peak in excess of 150 during week 4 pi, although intestinal mastocytosis persisted long after the loss of the majority of adult worms. Serum antibody responses to muscle stage larval antigen were detected in week 3 and increased subsequently. Both mastocytosis and antibody responses were more intense on secondary exposure to infection. Hamsters vaccinated with muscle stage larval antigen showed only a moderately accelerated loss of the intestinal phase but the fecundity of worms was severely suppressed. Overall it was concluded that the hamster host provided a model of trichinellosis that, in many respects was closer than mice and rats to the pattern of infection seen in economically and clinically important host species.
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PMID:The response of hamsters to primary and secondary infection with Trichinella spiralis and to vaccination with parasite antigens. 770 73

The mucosal mast cell and eosinophil responses of goats and sheep to a mixed gastrointestinal nematode infection were compared. Groups of eight does and nine ewes, previously maintained on pasture and treated with anthelmintic when they were housed and five worm-free lambs were challenged with 10,000 Trichostrongylus vitrinus third stage larvae (L3) and 10,000 Teladorsagia circumcincta L3. Eleven days after challenge, the ewes had significantly (P < 0.001) lower burdens of abomasal and intestinal worms than the does or naive lambs, but significantly higher (P < 0.001) tissue concentrations of mast cell proteinase. Toluidine blue-stained sections indicated a paucity of mast cells in the does compared with the ewes, whereas the immunolocalisation of sheep mast cell proteinase revealed similar numbers of stained cells in the two species. This discrepancy was due to the relatively high proportion of globule leucocytes (77 and 91 per cent in the jejunum and abomasum, respectively) in the does compared with the ewes (7 and 24 per cent in the jejunum and abomasum, respectively). No differences were detected between the numbers of circulating or tissue eosinophils in the ewes and does.
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PMID:A comparison of the mast cell and eosinophil responses of sheep and goats to gastrointestinal nematode infections. 770 60

The roles of IgE and mast cells on expulsion of adult Hymenolepis nana from the intestine were examined in mice. IgE-dependency was determined by comparing congenitally IgE-deficient SJA/9 and IgE-producing SJL/J mice infected with 50 H. nana eggs. Anti-H. nana IgE antibody was detected at three weeks post infection (p.i.) in SJL but not in SJA mice. The number of adult worms in the intestines of SJA and of SJL mice were similar at two weeks, but significantly more were found in SJA mice at three weeks p.i. Treatment of mice with anti-epsilon antibody also resulted in an increased worm burden at three weeks, suggesting participation of IgE in expulsion of H. nana. Intestinal mastocytosis was induced by infection regardless of the IgE status of the mice. Mast cell-dependency was tested in mast cell-deficient W/Wv and in normal littermate +/+ mice infected with 100 H. nana eggs. Anti-H. nana antibody was detected in both groups of mice at three weeks p.i. Worm expulsion seemed to be mast cell dependent because expulsion was less complete in W/Wv mice at three weeks p.i. Peripheral blood eosinophilia was comparable at three weeks p.i. in both IgE and mast cell sufficient and deficient mice. These results suggest that IgE and mast cells participate in the expulsion of H. nana adults from intestine in mice.
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PMID:Expulsion of Hymenolepis nana from mice with congenital deficiencies of IgE production or of mast cell development. 820 86

The possible importance of mucosal mast cells in the expulsive mechanisms of mice against Strongyloides venezuelensis was examined. After a primary infection by subcutaneous inoculation with various doses into C57BL/6 mice, about 50% of the initial dose of infective larvae (L3) became adult worms and, regardless of the dose of infection, they were completely expelled by Day 12 with similar kinetics. Intestinal mastocytosis at the time of expulsion was comparable among groups given different doses of infection. A kinetic study after infection with 2000 L3 in C57BL/6 mice revealed that mastocytosis started from Day 8, rapidly reached a peak on Day 12, and then gradually decreased. The strongest mastocytosis was observed in the upper one sixth of the small intestine where the majority of adult worms parasitized. Over 80% of mast cells induced by the infection were located in the intestinal epithelial layer. When mast cell-deficient W/Wv and their normal littermate +/+ mice were infected with 1000 L3, expulsion was significantly delayed in W/Wv mice, though adult worms were eventually expelled by Day 18 in W/Wv mice. Delayed expulsion as well as defective mast cell responses of W/Wv mice were completely restored by bone marrow grafting 10 weeks prior to infection. These results show that, like S. ratti infection, intestinal mucosal mast cells are important in causing expulsion of S. venezuelensis.
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PMID:Mucosal mast cells and the expulsive mechanisms of mice against Strongyloides venezuelensis. 822 56


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