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 effect of severe T-cell depletion on mucosal mast cells of the small intestine and on connective tissue mast cells has been studied in adult thymectomized, irradiated, bone marrow reconstituted (B) rats. Under normal conditions, intestinal mucosal mast cell numbers do not differ significantly between B rats, normal age matched rats and non-thymectomized irradiated controls. Connective tissue mast cells are significantly fewer in the tongues of B rats than in normal rats, but the difference is atributable to an effect of irradiation. Infestation with Nippostrongylus brasiliensis produced approximately equal increases in mucosal mast cells in non-thymectomized irradiation controls and in normal rats. In B rats there was no increase in mucosal mast cells following infestation. B rats failed to expel the parasites normally. Failure of mast cell proliferation was not due to the effects of the persisting worm burden. Antihelminthic treatment at the time of worm expulsion by normal rats did not reveal a hitherto masked mast cell response in B rats. Nippostrongylus infestation did not reveal evidence of thymus-dependency of connective tissue mast cells. As in athymic nude mice, mucosal mast cells in the rat have been shown to be T-cell dependent during the proliferation that follows infestation with an intestinal nematode parasite.
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PMID:Mast cells in severely T-cell depleted rats and the response to infestation with Nippostrongylus brasiliensis. 31 98

Although transcription of mast cell (MC) secretory granule neutral protease genes has been shown to distinguish MC subclasses in mucosal and serosal environments, the specific cytokines that regulate the expression of these genes have not been determined. To examine cytokine-mediated gene regulation, bone marrow-derived MC (BMMC) differentiated in vitro were obtained by culturing mouse bone marrow progenitor cells in the presence of WEHI-3 cell-conditioned medium, concanavalin A-stimulated splenocyte-conditioned medium (BMMCC), or recombinant (r) interleukin (IL)-3 (BMMCIL-3). All three populations of BMMC expressed the serosal MC-specific transcripts that encode mouse MC serine protease (MMCP)-5, MMCP-6, and MC carboxypeptidase A. However, only BMMCC contained MMCP-2 mRNA, a late expressed gene selectively transcribed by intestinal mucosal MC that proliferate during helminthic infestation in response to the T cell-derived cytokines IL-3, IL-4, and IL-10. When BMMCIL-3 were exposed to rIL-10 in the presence of either rIL-3 or rIL-4, they expressed MMCP-2 mRNA. Not only was the transcription of the MMCP-2 gene in BMMC dependent on continuous exposure of the cells to rIL-10, but the level of MMCP-2 mRNA in these cells could be down-regulated by rIL-3. These studies comparing the effects of two cytokines on the transcriptional regulation of secretory granule protease genes in MC demonstrate that rIL-10 induces BMMCIL-3 to express the mucosal MC protease MMCP-2, that rIL-3 attenuates the rIL-10-induced expression of this gene, and that transcription of the MMCP-2 gene is reversed in the absence of rIL-10.
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PMID:Transcriptional regulation of the mucosal mast cell-specific protease gene, MMCP-2, by interleukin 10 and interleukin 3. 156 97

Mast cell-deficient W/Wv mice and their mast cell-sufficient +/+ genetic controls were allowed to undergo three successive infestations with Dermacentor variabilis larvae. Histological examination of the skin of infected mice revealed large dermal accumulations of eosinophils and smaller numbers of neutrophils. The numbers of both eosinophils and neutrophils increased significantly in W/Wv and +/+ mice during secondary and tertiary infestations. Mast cell numbers were also found to increase in the skin of +/+ mice during tertiary infestations. Resistance, as measured by decreased larval engorged weights on day 5 of each infestation, was acquired by both strains of mice.
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PMID:Tick resistance in mast cell-deficient mice: histological studies. 186 63

Genetically mast cell-deficient (WB X C57BL/6)F1-W/Wv mice were used to investigate the role of mast cells for the acquisition of resistance against larval Haemaphysalis longicornis ticks. Resistance against ticks was evaluated by reduction in both number and weight of engorged ticks. Although (WB X C57BL/6)F1-+/+ mice with a normal number of mast cells acquired resistance after repeated infestation of ticks, the congenic W/Wv mice did not acquire it. Bone marrow transplantation from the +/+ mice were grafted onto the back of the W/Wv mice, resistance against the ticks was detectable in the grafted skin. In contrast, resistance was not detectable in the skin of the W/Wv mice which had been grafted onto the back of the syngenic W/Wv mice. Thus, we consider that the failure of the W/Wv mice to manifest resistance is attributable to the mast cell depletion.
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PMID:Inability of genetically mast cell-deficient W/Wv mice to acquire resistance against larval Haemaphysalis longicornis ticks. 389 1

The acquisition of resistance to ticks was monitored in mice of six different strains. Mice were subjected to repeated infestations with Dermacentor variabilis larvae, different skin sites being used for each successive infestation. In the third and fourth infestations, resistance was expressed in three strains of mice (WBB6F1-W/Wv, WBB6F1-+/+, and CFW), as demonstrated by significant reductions in percentages of larvae engorging and in mean weights of fed larvae. Both WBB6F1-W/Wv mice, which are mast cell-sufficient strain attained significantly higher levels of resistance. It is suggested that mast cells may play a relatively minor role in the mechanisms of resistance in this strain of mice. C57B1 mice also expressed tick resistance in their third and fourth infestations as measured by reduced percentages of engorged larvae, but not by reduced mean larval weights. Possibly, the mechanisms of tick resistance in this strain differ from those in other strains. Two other mouse strains (C3H-HeJ and C3H-HeSn) remained relatively susceptible to tick feeding throughout five infestations. In secondary infestations of all strains tested, no resistance was evident. Instead, enhanced feeding of larvae appeared to occur. A new objective measurement of tick resistance is the mean weights of detached, unengorged larvae taken from resistant animals at the end of the infestation period. These were found to be consistently less than those from susceptible animals.
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PMID:Dermacentor variabilis: resistance to ticks acquired by mast cell-deficient and other strains of mice. 397 57

The contributions of local and systemic factors to the regulation of mucosal mast cells and globule leukocytes have been examined in the rat. Nippostrongylus brasiliensis has been used to provide a potent immunological stimulus for mucosal mast cell hyperplasia and the roles of intestinal and extraintestinal sensitization observed by comparison of the gut mast cell responses to larval and adult worm infestations. Systemic effects of adult worm infestations have been examined in isolated Thiry-Vella loops of intestine. It is concluded that the extraintestinal phase of larval infestation is not obligatory for a gut mast cell response and that mast cell hyperplasia and globule leukocyte formation are not dependent on direct contact with the parasite or its products. The dissemination of the mast cell response and the general significance of the results are discussed.
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PMID:Local and systemic factors regulating mucosal mast cells. 686 62

Synthesis of specific homocytotropic antibody by cells from various lymphoid and haemopoietic organs in rats infested with Nippostrongylus brasiliensis has been studied by use of homologous adoptive cutaneous anaphylaxis and compared with the kinetics of appearance in the serum and thoracic duct lymph of specific IgE antibodies. Using this technique, synthesis of specific mast cell-sensitizing antibody has been detected in the draining lymph nodes of the lung as early as 12 days after infestation and by 14 days in the draining lymph nodes of the small intestine. Specific IgE antibody was not detected in serum until between 16 and 18 days after infestation. The delay in detection of antibody in the serum is at least in part due to its rapid removal from the blood, because antibody en route to the bloodstream from the gut-associated lymphoid tissue was detected in the thoracic duct lymph plasma as early as day 12. A major traffic of homocytotropic antibody-secreting cells has been detected in the thoracic duct lymph of the infested rats. The results are discussed in terms of the possible role of immediate hypersensitivity in the expulsion of the parasite, the origin of the IgE antibody response to the parasite and the mechanism of the potentiated reagin response.
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PMID:The distribution and traffic of specific homocytotropic antibody-synthesizing cells in Nippostrongylus brasiliensis-infested rats. Comparison of synthesis with the kinetics of antibody and IgE levels in serum and lymph. 697 8

In the reaction of Bos taurus cattle to infestation by the tick Boophilus microplus, mast cell histamine is translocated by the eosinophils to the attachment site. The concentration pattern of this cutaneous mediator for pain appears related to the grooming behaviour of the host.
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PMID:A putative role for eosinophils in tick rejection. 720 67

Infestation of larval Haemaphysalis longicornis ticks induced a threefold increase of eosinophils in the peripheral blood of normal WBB6F1- +/+ mice 2 days after tick infestation. In genetically mast cell-deficient WBB6F1- W/Wv mice, a threefold increase of blood eosinophils was observed 6 days after the tick infestation. However, marked infiltration of eosinophils was detected in the tick infestation sites of the WBB6F1- +/+ mice but not the WBB6F1- W/Wv mice. When the mast cell deficiency of WBB6F1- W/Wv mice had been rescued locally by intradermal injections of WBB6F1- +/+ mouse-derived cultured mast cells, a rapid increase of blood eosinophils and tissue infiltration of eosinophils were revealed following tick infestation. The intravenous (i.v.) injection of immune spleen or lymph node cells obtained from WBB6F1- +/+ mice 10 days after tick infestation led to significant eosinophilia in naive recipient mice. Treatment with anti-Thy-1.2 or anti-CD4 monoclonal antibody (mAb) and complement (C) completely abolished the eosinophilia; the early response (2 days after tick challenge) is dependent on mast cells at the feeding site, and the late response (6 days after tick challenge) is dependent on T lymphocytes. Since amplified interleukin-5 (IL-5) cDNA was detectable in the spleen cells 4 days after tick infestation, the late response might be mediated by IL-5. The infiltration of eosinophils at the feeding site of skin appeared to be dependent on mast cells.
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PMID:Mechanisms of eosinophilia in mice infested with larval Haemaphysalis longicornis ticks. 775 Oct 32

The effect of repeated infestations of Ixodes ricinus (L.) nymphs on BALB/c mice was studied. Four successive infectations resulted in an increase of tick feeding success. Tick yield and mean engorged weight increased and the length of the feeding period was reduced significantly (P < 0.05-0.01). The increase of specific anti-tick antibodies was not significant (P > 0.05). The blastogenic response of spleen lymphocytes to T-cell mitogens (Con A and PHA-P) was unimpaired or slightly enhanced, whereas the response to B-cell activators (LPS and PWM) was suppressed, as was the total antibody generation in vitro. The numbers of mast cells in murine skin at the tick attachment sites slightly decreased during the third infestation. The suppression of B-cell competence and of antibody generation, together with decrease of skin mast cell numbers in tick attachment sits, are considered to be responsible for enhancement of tick feeding success.
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PMID:Immunosuppression and feeding success of Ixodes ricinus nymphs on BALB/c mice. 778 20


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