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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cutaneous mast cells from 3 patients with mastocytosis were evaluated for their morphologic characteristics and in vitro functional reactivities to different secretory agonists. By electron microscopy, mastocytosis mast cells appeared larger than normal skin mast cells, frequently had atypical, highly indented or bilobed nuclei, and each contained numerous, elongated cytoplasmic projections. Suspensions of mastocytosis mast cells were obtained from lesional skin biopsy specimens, and their response to both immunologic and nonimmunologic secretagogues was compared with mast cells from normal skin. Lesional skin mast cells had a net histamine release of 12.3% (+/- 1.3 SEM) and 31.1% (+/- 6.0 SEM) following stimulation with the purified human anaphylotoxin C3a and mouse monoclonal antihuman IgE antibodies, respectively. This specific release was similar to the responses observed in normal skin mast cells (11.5% +/- 4.5 SEM and 16.7% +/- 2.1 SEM, respectively). Mast cells from cutaneous lesions of mastocytosis also responded to the nonimmunologic secretagogues, morphine sulfate and calcium ionophore A23187 with a specific histamine release of 15.1% (+/- 1.2 SEM) and 39.8% (+/- 8.7 SEM), respectively. The results of this study demonstrate that mast cells from lesions of mastocytosis are morphologically atypical, but have a histamine content similar to normal skin mast cells and retain their functional reactivities to clinically relevant secretory stimuli.
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PMID:In vitro functional reactivities of cutaneous mast cells from patients with mastocytosis. 362 98

Eosinophilia of synovial fluid is uncommon. Using the identification of Charcot-Leyden crystals to alert for the presence of eosinophils, we have increased by a factor of 5 the detection rate of synovial fluid eosinophilia. We describe here our clinical and laboratory findings in 7 patients with this feature. We believe they constitute a defined syndrome. Typically, the patients were young (ages 18-51) and had a personal and family history of allergy. They developed an acute, painless monarthritis after a minor trauma, and had no concurrent allergic symptoms. Each episode resolved in 1-2 weeks without therapy, and 3 patients had recurrences. All had pronounced dermatographism. The synovial fluid was mildly inflammatory: 10,850 +/- 3,665 white blood cells/mm3, with 41 +/- 5% eosinophils (mean +/- SEM). The cellularity and chemistry of the peripheral blood was unremarkable, except for a mild elevation of IgE levels (370 +/- 104 IU/ml). The exact pathophysiologic mechanism underlying this benign entity is not clear, but we suspect a nonimmunologic triggering event is operant, i.e., synovial trauma which mimics the cutaneous dermatographism.
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PMID:Eosinophilic synovitis: clinical observations on a newly recognized subset of patients with dermatographism. 375 40

We have studied 26 patients with asthma who had positive skin tests for Bermuda grass pollen antigen (BGP) with history, immunologic assays, and bronchial challenge with BGP. In these patients IgE anti-BGP RAST titers were higher in those with positive, 6.8 +/- 4.4% (mean +/- SEM) compared to those with negative bronchial challenges, 2.7 +/- 0.4% (p less than 0.02). Historical data did not predict bronchial challenge response. IgG4 anti-BGP RAST was not different in patients with positive and negative challenges but was markedly increased, 15.3 +/- 11.9%, in patients who had previously had BGP immunotherapy when compared to untreated patients, 3.6 +/- 5.1% (p less than 0.01). IgE anti-Bermuda grass appears to be the major contributor to susceptibility to BGP bronchial challenge. IgG4 anti-Bermuda grass is apparently unrelated to the sensitivity to challenge but appears to be a significant component of the immunologic response to immunotherapy.
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PMID:Immunologic and clinical correlates of bronchial challenge responses to Bermuda grass pollen extracts. 387 47

We studied the responses to antigen in animals selected from a colony of inbred dogs sensitized to specific allergens to determine if they had characteristics similar to those of human asthmatics. They were immunized with ragweed and grass pollen extracts (10 micrograms in alum) immediately after routine vaccination with attenuated live virus (distemper and hepatitis) and killed bacteria (Leptospira) at 4, 8, and 12 wk of age. Subsequently, ragweed and grass injections were repeated every 2 months. Immunized dogs made specific IgE-antibodies in serum averaging 3 to 4 times that of control animals (no immunization with pollen or vaccine). They showed positive skin responses to the injection of ragweed pollen extract, whereas control dogs did not respond to ragweed pollen by quantitative skin test or inhalation challenge. In immunized dogs under barbiturate anesthesia, air-flow resistance of the total respiratory system increased from 0.60 +/- 0.07 (mean +/- SEM) before to 12.6 +/- 3.4 cm H2O/lps 5 min after the start of antigen aerosol; respiratory resistance remained increased for 20 min and was associated with 0 hypoxemia and increased arterial plasma histamine. In addition, airway responsiveness to both inhaled histamine and methacholine was greater in immunized dogs than in nonimmunized dogs of comparable age. Airway responses to each agonist were highly reproducible on repeated testing. These results indicate that physiologic responses to antigen by inbred, ragweed-sensitized dogs resemble human asthma closely and that these dogs appear suitable for a variety of experimental studies of asthma with respect to pathogenesis, diagnosis, prevention, and treatment.
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PMID:Airway responsiveness to inhaled antigen, histamine, and methacholine in inbred, ragweed-sensitized dogs. 389 78

We investigated the ability of antigen-IgE interactions to stimulate histamine release from human infant cutaneous mast cells. Skin obtained at circumcision contained numerous perivascular mast cells, as assessed by light and electron microscopy. The histamine content of this tissue averaged 17.7 ng (+/- 1.5 SEM)/mg wet weight. Challenge of 200-microns thick sections of unsensitized skin with varying concentrations of monoclonal murine antibodies to human IgE caused no net release of histamine. After skin sections were incubated in the presence of 5 micrograms/ml of human myeloma IgE (S) for 120 min at 37 degrees C, monoclonal anti-IgE challenge resulted in 40.1% (+/- 6.0 SEM) histamine release. Similar passive sensitization with 1/20 dilutions of serum from humans expressing IgE to purified Juniperus sabinoides (JS) antigen rendered the tissue responsive to specific antigen challenge. Dose-related histamine release occurred over 30 min with optimal release of 12.6% (+/- 2.4 SEM) after stimulation with 100 ng/ml of JS antigen. This reaction required sensitization with serum containing IgE to JS and was antigen-specific. Optimal reactions to antigen occurred at 3 mM added Ca++, 34 degrees C to 37 degrees C, pH 7.2. Antigen-induced release was markedly influenced by the added Ca++ concentration; no release occurred in the absence of Ca++, 54% of the optimal response was observed at 2 mM Ca++, and 28% of the optimal response occurred at 4 mM Ca++. The addition of Mg++ did not influence antigen-induced release. The results of this study provide functional evidence that 1) human infant cutaneous mast cells express Fc-epsilon receptors; 2) these receptors are largely unoccupied in vivo; and 3) stimulation of passively sensitized infant mast cells with anti-IgE or specific antigen leads to immediate histamine release. This new system should permit detailed in vitro studies of immediate hypersensitivity reactions in human skin.
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PMID:IgE-mediated release of histamine from human cutaneous mast cells. 618 24

We determined the histamine content in the skin of 22 adults with atopic dermatitis, one patient with hyper-IgE-syndrome, and 20 controls by the enzymatic double isotope assay. In addition, we performed a pilot study of histamine degradation in the skin. We tested, furthermore, the releasability of histamine from skin sections of patients with atopic dermatitis and healthy controls upon challenge with acetylcholine, anti-IgE, and compound 48/80. Histamine was also determined in 13 plasma specimens and was always less than 1 ng/ml. The mean +/- SEM histamine concentration in the skin was 196 +/- 30 ng/mg protein in controls and 262 +/- 68 ng/mg protein in atopic dermatitis (no statistically significant difference). One control and three patients with atopic dermatitis exhibited a slight, the hyper-IgE patient a marked, elevation of the skin histamine content. No gross differences in the degradation rate of histamine were observed between patients and controls. Acetylcholine and 48/80 induced the same histamine release in both groups; with anti-IgE, almost the double amount of histamine was released from the skin of atopic dermatitis patients as compared to controls. These findings suggest an enhanced releasability of histamine upon immunologic challenge in atopic dermatitis.
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PMID:Cutaneous histamine levels and histamine releasability from the skin in atopic dermatitis and hyper-IgE-syndrome. 618 56

The membrane potential of rat basophilic leukemia cells (RBL-2H3 cell line) has been determined by monitoring the distribution of the lipophilic [3H] tetraphenylphosphonium cation between the cells and the extracellular medium. By this method, the determined potential of these cells, passively sensitized with IgE, is -93 +/- 5 mV (mean +/- SEM, interior negative). Almost 40% of this membrane potential is rapidly collapsed upon the addition of the proton carrier, carbonyl cyanide p-trifluoromethoxyphenyl hydrazone (FCCP). It is suggested that the FCCP-sensitive fraction of the total membrane potential results from the accumulation of this cation by the mitochondria, which maintains a negative membrane potential. Thus, the resting plasma membrane potential of these cells equals -55 +/- 6 mV. During the process of immunological stimulation by antibodies directed against cell membrane bound IgE, the membrane potential decreases. Moreover, there is a correlation between the extent of degranulation of the cells and the depolarization. It is concluded that in common with other secretory systems, depolarization of the plasma membrane is involved in the stimulus-secretion coupling of the histamine secreting RBL cells.
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PMID:Membrane potential changes during IgE-mediated histamine release from rat basophilic leukemia cells. 619

The effect of auranofin, an oral chrysotherapeutic agent, on histamine release from human basophils was studied. Auranofin inhibited IgE-mediated, anti-IgE-induced histamine release in a dose-dependent fashion with a concentration of drug required to produce 50% inhibition of 1.3 micrograms/ml. This compound also inhibited calcium ionophore A23187 and 12-0-tetradecanoyl-phorbol-13-acetate-induced histamine release with a concentration of drug required to produce 50% inhibition of 1.7 micrograms/ml and 0.9 micrograms/ml, respectively. Auranofin was less active for formyl-L-methionyl-L-leucyl-L-phenylalanine-induced release of histamine with 32 +/- 10% (mean +/- SEM) inhibition at 2 micrograms/ml. Auranofin effects were reversible when leukocytes preincubated with auranofin was washed with buffer. In contrast, gold sodium thiomalate enhanced IgE-mediated histamine release, suggesting that these two compounds exert their actions at different levels. These results suggest that auranofin may be beneficial to patients with allergic diseases such as bronchial asthma.
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PMID:Auranofin, an oral chrysotherapeutic agent, inhibits histamine release from human basophils. 620 6

We present a colony assay system that allows in situ identification of human basophil/mast cell (basophil) colonies. In methylcellulose culture, in the presence of phytohemagglutinin-leukocyte conditioned media (PHA-LCM), human peripheral blood and bone marrow cells form colonies that can be distinguished by their unique morphological characteristics. Pure basophil colonies are diffuse, small colonies containing small, round, highly refractile cells. These characteristics of the constituent cells led us to the observation that a significant number of basophils are found in combination with eosinophils. The mixed eosinophil/basophil colonies have the distinctive elements of pure eosinophil and pure basophil colonies. Usually, these are diffuse colonies with compact clusters of slightly larger, darker-appearing cells. We also found colonies that contained basophils and neutrophils/monocytes, but this type could not be consistently identified by in situ morphology. Cytochemical analysis confirmed the metachromatic nature of the granules in the basophils. The presence of IgE receptors on the cells was documented by indirect immunofluorescent staining after passive sensitization with purified human IgE. Peripheral blood cells from six healthy volunteers formed 5.7 +/- 1.0 (mean +/- SEM) pure colonies in 2 X 10(5) cells. Cultures of bone marrow cells from patients with various types of anemia had 9.0 +/- 1.5 colonies in 10(5) cells. This is the first description of a colony assay system for in situ identification of a pure population of basophilic granulocytes.
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PMID:Identification of pure and mixed basophil colonies in culture of human peripheral blood and marrow cells. 623 38

Eosinophilia within the first 6 weeks of life was studied prospectively in 10 premature neonates. Mean birthweight was 1229 +/- 314 g, and mean gestational age 31.5 +/- 1.8 weeks. Simultaneous changes in eosinophil, neutrophil, total lymphocyte, suppressor and helper T-cell counts and IgE levels were monitored. Infants were designated as responders (eosinophils greater than 1000/microliter for greater than 5 days) and non-responders. In the 6 responders eosinophils increased from 353 +/- 76 (mean +/- SEM) at birth to a peak of 2783 +/- 430/microliter at 20-25 days. Responders had significantly lower neutrophil counts at birth (P less than 0.05), and in 5 of the 6 responders neutrophils increased by more than 100% within 10-15 days; this did not occur in any of the 4 non-responders (P less than 0.025). Lymphocytes and suppressor and helper T cells increased progressively in both groups over the period of study with no differences between responders and non-responders. Birthweight and gestational age were similar in both groups, and there were no apparent causes for the lower neutrophil counts in responders at birth. Eosinophilia was not related to an IgE response. The incidence of eosinophilia in this study is similar to that reported previously, and appears to be part of a biphasic granulopoietic response.
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PMID:Eosinophilia in premature neonates. Phase 2 of a biphasic granulopoietic response. 662 38


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