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)

In vivo studies have shown that human C5a, a potent complement-derived anaphylatoxin and chemoattractant, produces immediate inflammatory reactions following intradermal injection in human skin. At concentrations within its potential physiologic range, intradermal injection of C5a elicits immediate wheal and flare reactions, increased vascular permeability, mast cell degranulation, and neutrophil-rich infiltrates. To assess the relative contribution of interacting cellular elements to C5a-induced inflammation in normal human skin, purified human C5a was tested intradermally in 8 patients with bone marrow failure (BMF). Reactions to C5a in patients with BMF were compared with responses at identical test sites in healthy volunteers and other patients with cutaneous disorders. Patients with BMF demonstrated significantly less wheal and flare reactivity following intradermal injection of C5a than controls (p less than 0.05 and less than 0.02, respectively). In these studies, patients with the greatest cytopenia generally showed the least cutaneous reactivity to human C5a. Biopsies of C5a test sites in patients with BMF revealed an absence of leukocytes in marked contrast to neutrophil-rich infiltrates observed at test sites in healthy volunteers. Avidin-fluorescent and/or Giemsa staining of skin biopsies revealed no difference between the number of dermal mast cells in patients with BMF and samples of normal human skin. In addition, skin test studies with histamine (2 micrograms) and morphine (5 micrograms) performed to assess cutaneous vascular and mast cell responsiveness in patients with BMF, normal volunteers and controls with rhinitis revealed no significant differences in cutaneous reactivity to these pharmacologic agents. These in vivo studies demonstrate that patients with BMF specifically exhibit decreased cutaneous reactivity to human C5a and suggest that neutrophils make an important and an immediate contribution to inflammatory responses elicited by this anaphylatoxin.
J Invest Dermatol 1987 Apr
PMID:Patients with bone marrow failure demonstrate decreased cutaneous reactivity to human C5a. 355 64

In order to evaluate mast cell participation in allergic contact hypersensitivity (ACH), BALB/c mice were sensitized with 0.1% trinitrochlorobenzene (TNCB). Immediately before challenge and at 1, 1.5, 2, 4, 6, 8, 12, 24, and 48 h after challenge with 1% TNCB, groups of animals had ear thickness measured, had blood collected for histamine determinations, and had both ears removed for histologic evaluation of mast cells. The increase in ear swelling was triphasic with peak increases at 1.5 h (14.3 +/- 1.6 X 10(-2) mm; mean +/- SEM), 8 h (19.9 +/- 1.8 X 10(-2) mm), and 24 h (30.2 +/- 2.9 X 10(-2) mm). A triphasic pattern of increased serum histamine was noted at 1-4 h (117% over control levels), at 12 h (131%), and at 48 h (133%). Examination of the tissue specimens from challenged animals showed modest (1+) degranulation of mast cells between 1 and 6 h with extensive (2+) degranulation at 12 h. In addition, hypogranulated mast cells were evident between 1 and 6 h, at 24 h, and at 48 h. There were no statistically significant differences in mast cell numbers at any time. Neither platelets nor other formed elements of the blood contributed to the increased blood histamine levels. These data show that mast cells are activated in a triphasic pattern during ACH, and thus suggest both early and late roles for the mast cell and its products in the evolution of ACH.
J Invest Dermatol 1987 Jun
PMID:Mast cell participation during the elicitation of murine allergic contact hypersensitivity. 358 52

An urticarial dermatosis after contact with the urticating hairs of the adult female Hylesia moth may occur by several mechanisms including the intradermal injection of inflammatory mediators through the urticating hairs. Extracts were prepared from whole moths, urticating hairs, and other moth parts. Each of these extracts was subjected to a radioenzyme assay for histamine. Histamine was present in extracts made from whole moths and from urticating hairs. Extracts made from other moth parts contained no histamine. Cutaneous wheals occurred after intradermal injections of histamine and various concentrations of Hylesia extract (HE) into the backs of cynomolgus monkeys. This whealing response was suppressed by pretreatment of the animals with diphenhydramine hydrochloride, but not by pretreatment with indomethacin. Histologic examinations showed a perivascular lymphocytic infiltrate around dilated capillaries without evidence of mast cell degranulation in HE-injected sites but not in controls. These findings provide evidence that histamine may be the mediator responsible for the urticarial lesions seen after contact with Hylesia moths.
J Invest Dermatol 1987 Jun
PMID:Evidence for histamine in the urticating hairs of Hylesia moths. 358 53

The role of IgG4 in atopic dermatitis was investigated by determining the total amounts of IgG4 and of IgG4 specific for ovalbumin (a food allergen), Dermatophagoides farinae mite antigen and house dust (inhalant allergens) and Candida. These were related to the amounts of total and antigen specific IgE in patients with atopic dermatitis and normal healthy controls. Most patients with atopic dermatitis had greater amounts of total IgG4 and of antigen-specific IgG4 than did normal control individuals. Patients who had received hyposensitization treatment injections had greater amounts of IgG4 than the atopic dermatitis patients not so treated. In patients treated by hyposensitization there was a large increase in the amount of blocking antibody detected by incubating the antigen with the serum overnight before injecting the mixture into the skin of a patient sensitive to the antigen. Blocking activity was also examined by partial inhibition by the serum of IgE-mediated mast cell degranulation and by injection of serum into the skin of sensitive patients before challenge with antigens. In all tests the blocking activity of the serum was related to the amount of antigen-specific IgG4 but not related to total IgG4. In patients with atopic dermatitis who were sensitive to mite antigen, severe cases had small amounts of specific IgG4 and large amounts of specific IgE but in mild cases there was an opposite trend with relatively large amounts of specific IgG4. Large amounts of IgG4 ovalbumin specific antibody were found in children and adults with atopic dermatitis and egg allergy but small amounts of IgE. In infants most of the anti-ovalbumin antibody was IgE with little or no IgG4. The work of others has confirmed that increased amounts of total and antigen-specific IgG4 occur in atopic dermatitis, and it is concluded that IgG4 is a blocking antibody for anaphylactic sensitization responses.
Br J Dermatol 1987 Sep
PMID:IgG4 antibodies in patients with atopic dermatitis. 367 80

Acute cutaneous photosensitivity is a major manifestation of certain forms of human porphyria and also occurs in patients treated with hematoporphyrin derivative (HpD) photoradiation for the diagnosis and treatment of malignant tumors. In this study a quantitative animal model useful for in vivo studies of acute porphyrin photosensitization in cutaneous tissue was developed. C3H mice injected with HpD and irradiated 6 h later with 405 nm energy developed a 40-90% increase in ear thickness which was present immediately after irradiation and persisted for at least 24 h. No ear swelling occurred in animals receiving 405 nm radiation alone or HpD alone. Histologically, this photosensitivity reaction was manifest as edema, vascular dilatation, and mast cell degranulation immediately after irradiation followed by an influx of polymorphonuclear leukocytes and epidermal necrosis 24 h later. Tissue injury evoked by HpD and light was accompanied by extravasation of intravenously administered 125I-labeled albumin in the irradiated ears, indicating that photosensitization was accompanied by transudation of serum into the site of tissue injury. An in vivo correlation of this approach was verified by detection of measurable increase in ear thickness in irradiated mice rendered porphyric by the ingestion of a griseofulvin-containing diet. The mouse ear swelling model offers a useful system with which to study acute porphyrin photosensitization in the skin, and may lead to important new insights into the pathogenesis and prevention of this form of phototoxicity.
J Invest Dermatol 1986 Jun
PMID:Cutaneous porphyrin photosensitization: murine ear swelling as a marker of the acute response. 371 77

The involvement of mast cells in the elicitation of contact photosensitivity (CPS) was examined in mice treated with pharmacologic agents and in genetically mast cell-deficient W/Wv mice. Contact photosensitivity responses were diminished by pretreatment with reserpine, which may have been due to depletion of vasoactive amines in mast cells. This inhibition was almost reversed by the monoamine oxidase inhibitor, pargyline-HCl, which prevented reserpine-induced depletion of vasoactive amines such as serotonin. Defective CPS was also found in W/Wv mice, but not in their congenic littermates (+/+). Abnormal CPS in mast cell-deficient mice was due to a defect in the elicitation of CPS rather than a defect in the induction of effector T cells, since the ability to elicit CPS could be transferred to normal +/+ mice by photosensitized cells from mast cell-deficient mice. These findings favor the view that mast cells are involved in the elicitation of CPS.
J Invest Dermatol 1986 Jul
PMID:Mechanisms of contact photosensitivity in mice. VII. Diminished elicitation by reserpine and defective expression in mast cell-deficient mice. 372 61

We report a patient with cholinergic urticaria in whom stroking the skin produced a band of erythema studded with the small weals characteristics of cholinergic urticaria. This response was suppressed by pre-treatment with topical scopolamine. Light and electron microscopy of the weal showed mast cell degranulation and a moderate mononuclear cell infiltrate.
Br J Dermatol 1986 Sep
PMID:Cholinergic dermographism. 375 94

Aquagenic pruritus is a disease in which itchy prickling skin discomfort is evoked by contact with water at any temperature without observable cutaneous lesions. Little is known about its etiology and pathogenesis. Previous reports show that increased levels of blood histamine and cutaneous mast cell degranulation are present before water exposure and that they increase still further with water challenge. This paper shows that fibrinolytic activity is markedly increased both before and after water exposure, while circulating fibrinolytic activity is normal before water exposure in three cases of aquagenic pruritus. A patient who was asymptomatic at the time of the study had no observed increase in fibrinolytic activity either before or after water challenge, suggesting that the remission of symptoms of aquagenic pruritus and normalization of cutaneous fibrinolytic activity are interdependent factors.
Int J Dermatol 1986 Oct
PMID:Increased cutaneous fibrinolytic activity in aquagenic pruritus. 377 Oct 51

This study was designed to investigate the effect of middle-wave ultraviolet (UVB) radiation on mast cell functions using mouse ear skin as an in vivo model. Groups of UVB-irradiated BALB/c mice were given an intradermal injection of the mast cell degranulator compound 48/80 into ears at various time intervals (30 min-7 days) after a single exposure to a bank of fluorescent sunlamp tubes (10-100 mJ/cm2). Both the compound-evoked ear swelling response (ESR) and mast cell degranulation were significantly suppressed by preexposure to UVB (25-100 mJ/cm2) after 0 (30 min) to 3 days postirradiation, with a subsequent recovery by day 7. No such effects were observed in mice irradiated with 10 mJ/cm2. The ESR induced by 5-hydroxytryptamine was not significantly affected by UVB radiation during the experimental period. While within this dose range UV radiation itself caused neither loss of mast cell counts nor a measurable degree of degranulation in ear skin, exposure to larger amounts of UV energy (200-500 mJ/cm2) produced tremendous ear swelling with histologic features of mast cell degranulation in an early phase of inflammation. The results suggest that UVB radiation exerts a dual effect on mast cells and that administration of smaller amounts of UVB may alter the mast cell/vasoactive amine system, suppressing ear swelling in response to the degranulator. Vascular reactivities to vasoactive amines were not affected by UVB irradiation.
J Invest Dermatol 1986 Dec
PMID:Ultraviolet-B radiation suppresses mast cell degranulation induced by compound 48/80. 378 60

Numbers of mast cells were quantitated in the lesions of diffuse scleroderma and morphea. Mast cells increased and then decreased in number in the papillary dermis of diffuse scleroderma. No significant change of mast cell numbers was noted in the reticular dermis. Mast cells increased in the papillary dermis with fine collagen bundles (grade 2 skin of scleroderma) and decreased in the papillary dermis with homogeneous collagen bundles (grade 3 skin of scleroderma). The total number of cells increased in the papillary dermis of grade 1 and 2 skin of scleroderma and decreased in the grade 3 skin of scleroderma. In morphea a reduced number of mast cells was noted in grade 3 lesions. It is suggested that mast cells play an important role in fibrotic process of scleroderma skin.
Arch Dermatol 1987 Feb
PMID:Mast cell numbers in diffuse scleroderma. 381 93


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