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Biomedical subjects

W W Busse

Publications and source records attributed to W W Busse.

At least 235 records · Page 13Linked to original sources
PubMed1979

Impairment of isoproterenol, H2 histamine, and prostaglandin E1 response of human granulocytes after incubation in vitro with live influenza vaccines.

The release of the lysosomal enzyme beta-glucuronidase from granulocytes follows incubation in vitro with complement-activated zymosan particles. Release of beta-glucuronidase is inhibited by isoproterenol, histamine, and prostaglandin E1. This in vitro model was used to study the effect of incubating a live, bivalent (A + B) influenza vaccine on the granulocyte response to the agonists described. After incubation in vitro with the live, bivalent influenza vaccine, there was a significantly impaired granulocyte reponse to all 3 agonists. The change in the response of polymorphonuclear leukocytes to isoproterenol was similar to an impairment in beta-adrenergic response found during respiratory infections in vivo. The viral-induced changes in the granulocyte response to isoproterenol may reflect similar alteration in other tissues, such as variable control of the airways and provide one explanation for the occurrence of airway dysfunction during respiratory infections.

Adult↗
PubMed1978

The use of the radioallergosorbent test in the diagnosis of Hymenoptera anaphylaxis.

IgE antibody levels to Hymenoptera (honey bee, hornet, wasp or yellow jacket) venom or venom sac were measured in the serum of ninety-six patients with a history of immediate hypersensitivity reactions to these insect stings. Normal levels of IgE antibody were found in fourty-four of these patients tested. The severity of the systemic reaction was similar in those patients with normal and elevated IgE antibody levels, and the interval from the systemic reaction to antibody determination was also similar. In twelve patients with a definite reaction to honey bee venom, the IgE antibody was elevated in all and correlated with a positive venom skin test in nine out of the twelve. It is not possible to determine if the other patients with normal IgE antibody and a systemic reaction represent a false negative RAST value, loss of sensitivity to the Hymenoptera venom, or a lack of RAST sensitivity with some venom or venom sac antigens. Without the ready availability of venom skin tests to all Hymenoptera antigens or other in vitro tests, a definite assessment of insect anaphylaxis remains in doubt for the patient and physician.

Adolescent↗
PubMed1978

Response to corticosteroids in the hypereosinophilic syndrome. Association with increased serum IgE levels.

Severe blood eosinophilia (16,500/cu mm and 6,500/cu mm) accompanied by involvement of the lungs, pleura, heart, pericardium, liver, gastrointestinal tract, peripheral nerves, or skin developed in two patients with bronchial asthma. Associated with the eosinophilia were elevated serum IgE levels (1,400 IU/ml and 10,500 IU/ml), depressed serum C4 complement levels (13 mg/100 ml and 6 mg/100 ml), and high titers of rheumatoid factor (1:2560 and 1:640). Symptoms improved after treatment with prednisone and the eosinophil counts and serum IgE and C4 complement levels returned to normal.

Asthma↗
PubMed1977

Effect of beta adrenergic agonist, prostaglandins, and cortisol on lymphocyte levels of cyclic adenosine monophosphate and glycogen: abnormal lymphocytic metabolism in asthma.

Decreased beta adrenergic regulation of cyclic adenosine monophosphate (cAMP) in lymphocytes has been described in asthma. We investigated adrenergic stimulation of glycogenolysis and responses to prostaglandin E1 (PGE1). Lymphocytes from 24 normal and 24 mild asthmatic subjects who had no drugs for at least 2 weeks were separated on Ficoll-hypaque and incubated in medium 199 with Hepes buffer. Beta adrenergic stimulation of cAMP and glycogenolysis was reduced in the asthmatics (p less than 0.05). PGE produced less of a rise in cAMP in asthmatics than in normals, but the difference was not significant (p greater than 0.05) and glycogenolysis was normal. Cortisol added in vitro potentiates the effect of isoproterenol and PGE1--but in the presence of cortisol the response of the asthmatic cells to isoproterenol is still lower than that of normal cells. This observation would support that "beta adrenergic blockade" is the major defect of asthmatic cells. The conclusion is further supported by the observation that the degree of the blockade is associated with a pathologic condition.

Adrenergic beta-Agonists↗
PubMed1977

Decreased granulocyte response to isoproterenol in asthma during upper respiratory infections.

Isoproterenol inhibits zymosan-stimulated release of lysosomal enzymes from granulocytes. Using this as an in vitro cell model to study beta-adrenergic response, granulocyte reaction to isoproterenol was examined in asthma. There was a significantly decreased response to isoproterenol (10(-7) to 10(+-5) M) in patients with mild asthma who had not taken bronchodilators for 2 weeks before study and also in patients with severe asthma requiring bronchodilators and corticosteroids. During respiratory infections that provoked an attack of asthma, the granulocyte response to isoproterenol was further decreased. The change in granulocyte response to isoproterenol may reflect a similar change in beta-adrenergic tone of the airways and provide one explanation for asthma during colds.

Adult↗
PubMed1977

Decreased H2 histamine response of granulocytes of asthmatic patients.

Increased bronchial sensitivity to inhaled histamine in asthma is well known. The mechanism of this increased bronchial sensitivity is not known nor has it been demonstrated that isolated cells respond abnormally to histamine. Polymorpho-nuclear leukocytes (PMNs) provide a homogeneous cell population to study agonist response. Release of granulocyte lysosomal enzymes is inhibited by agonists increasing the PMN cyclic AMP concentration. The release of the lysosomal enzyme beta glucuronidase by serum-activated particles of zymosan was similar in PMNs isolated from normal and asthma subjects. Histamine (100-0.01 muM) inhibited enzyme release. Except at the maximal concentration of histamine (100 muM), the response to histamine was decreased in asthma. The inhibition of enzyme release paralleled an increase in intracellular PMN cyclic AMP. In asthma, the cyclic AMP response to histamine was reduced. The H2 antihistamine metiamide blocked histamine inhibition of lysosomal enzyme release and the increase in cyclic AMP. The effect was maximal at concentrations equimolar to those of histamine. The H1 antihistamine chlorpheniramine had no effect on histamine inhibition of granulocyte lysosomal enzyme release. A decrease in the inhibition of the release of the inflammatory lysosomal enzymes from granulocytes in asthma may contribute to an enhanced bronchial inflammatory reaction.

Adult↗
PubMed1976

Histamine inhibition of neutrophil lysosomal enzyme release: an H2 histamine receptor response.

Human polymorphonuclear leukocytes treated with cytochalasin B release the lysosomal enzyme beta glucuronidase during contact with serum-activated zymosan particles. Histamine increases intracellular cyclic adenosine monophosphate and inhibits release of this enzyme. The H2 antihistamine metiamide blocks the histamine inhibition of lysosomal enzyme release and the increase in the intracellular adenoisine 3,5'-monophosphate of granulocytes. Chlorpheniramine, an H1 antihistamine, did not block the histamine inhibition of granulocyte lysosomal enzyme release.

Cyclic AMP↗
PubMed1976

Alternaria IgG precipitins and adverse reactions.

Late reactions consisting of fever, malaise, and swelling at the site, 4 to 6 hr after injections of Alternaria extract occurred in several patients receiving immunotherapy with Alternaria. These patients had in common serum IgG precipitins and exquisite leukocyte histamine release sensitivity to Alternaria. Such precipitins were 3 times more frequent in patients receiving Alternaria immunotherapy than a control group of patients receiving immunotherapy with other antigens. A prospective study revealed that 5 of 23 Alternaria-sensitive persons had precipitins before immunotherapy and another 6 developed precipitins during therapy. Only one of the 23 experienced a late Alternaria reaction. Thus, precipitins to Alternaria are common and do not seem to be the basis for the late reactions we observed. The finding of precipitins does not contraindicate immunotherapy.

Alternaria↗
PubMed1976

Intranasal immunization with attenuated live influenza vaccine in asthma.

Attenuated live intranasal influenza vaccine ("Alice") was given to 20 asthmatics and 9 control subjects. Pulmonary function were performed before and after, with emphasis on tests of small airways function (using flow volume curves with air and a helium-oxygen mixture). In subjects with a low influenza A antibody titer, there was a 4-fold rise in titer to the vaccine, whereas those subjects with a high titer showed no rise. There were no significant changes in pulmonary function in any parameters measured, and no significant symptoms were reported. We have concluded from this study that "Alice" appears safe for use in asthma and was capable of producing an antibody titer rise in persons with low titers.

Administration, Intranasal↗
PubMed1976

Decreased adrenergic responses in lymphocytes and granulocytes in atopic eczema.

The physiologic and cyclic adenosine monophosphate (cAMP) response to beta adrenergic stimulation in lymphocytes and granulocytes was examined in atopic eczema. These cells were isolated by Ficoll-Hypaque gradient from 10 patients with atopic eczema, and their responses were compared to 10 normal subjects. In eczema, basal concentrations of cAMP were normal in both lymphocytes and granulocytes. Lymphocyte cAMP response in eczema was decreased both to epinephrine (10-5 M) and to isoproterenol (10-5 M) but normal to prostaglandin E1 (PGE1). It was also noted that the glycogenolysis response to isoproterenol was significantly less at 10-5 M in eczema, but the fall in glycogen was normal with PGE (10-5 M and 10-7 M). The inhibition of lysosomal enzyme release from granulocytes after zymosan stimulation was significantly less (p less than 0.01) in eczema with all concentrations of isoproterenol tested. There was also a decrease in cyclic AMP response to isoproterenol in the polymorphonuclear leukocytes. PGE1 inhibited lysosomal enzyme release and stimulated cAMP normally. In eczema, both lymphocytes and polymorphonuclear leukocytes have a decreased beta adrenergic response.

Adolescent↗
PubMed1976

Adrenergic mechanisms and the adenyl cyclase system in atopic dermatitis.

Patients with atopic dermatitis have abnormal autonomic responses of the arterioles, pilomotor smooth muscle, and sweat glands. Their lesions have been reported to contain increased amounts of the neurohumors, acetylcholine and norepinephrine, as well as increased activity of acetylcholinesterase and catechol-O-methyltransferase. In vitro studies of epidermis show that beta adrenergic agonists fail to evoke the normal inhibition of mitosis of basal cells of patients with atopic dermatitis. Epidermis removed not only from the lesions, but also from normal-appearing skin, responded abnormally. The increase in intracellular levels of cAMP after exposure to catecholamines was similar in normal and atopic epidermis. Lymphocytes and PMN leukocytes isolated from patients with atopic dermatitis show both a decreased physiologic response (glycogenolysis and inhibition of lysosome enzyme release) and a decreased rise in intracellular levels of cAMP upon incubation with beta agonists, but a normal response to PGE1. Cortisol increases the response of lymphocyte adenyl cyclase to both agonists and, in the case of the patients with atopic disease, more than overcomes the depressed response to beta agonists. Because the leukocytes respond normally to PGE1 and because others have reported normal activities of skin and adenyl cyclase, phosphodiesterase, and protein kinases, we conclude that the step responsible for the diminished beta adrenergic response lies antecedent to the catalytic site of adenyl cyclase.

Acetylcholine↗
PubMed1975

Immunotherapy in bee-sting anaphylaxis. Use of honeybee venom.

After nine months of immunotherapy with commercially prepared wholebody bee extract, a beekeeper's wife experienced anaphylaxis after a controlled bee-sting challenge. High risk of future bee stings prompted a decision to attempt desensitization with honeybee venom. This was extracted from the bee into Coca solution and administered parenterally in increasing daily doses until an equivalent of one venom sac was given per day. This maintenance dosage was continued for a month. Anaphylaxis did not occur after another bee-sting challenge. Therapy has been maintained with venom. With this treatment, there has been an increase in the level of IgG-blocking antibody and a fall in IgE titer to bee venom (radioallergosorbent test [RAST]).

Adult↗
PubMed1975

Asthma from psyllium in laxative manufacture.

Symptoms of asthma developed in three patients after exposure to psyllium powder, which was being used in the manufacture of a bulk laxative. All three had reaginic skin test sensitivity, and two had positive bronchial challenges with a psyllium extract.

Adult↗