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Biomedical subjects

W W Busse

Publications and source records attributed to W W Busse.

At least 199 records · Page 11Linked to original sources
PubMed1985

Soybean oil is not allergenic to soybean-sensitive individuals.

We have previously demonstrated that peanut oil is not allergenic to peanut-sensitive individuals. Seven soybean-sensitive patients were enrolled in a double-blind crossover study to determine whether ingestion of soybean oil can induce adverse reactions in such patients. All subjects had histories of systemic allergic reactions (urticaria, angioedema, wheezing, dyspnea, and/or vomiting) after soybean ingestion and had positive puncture skin tests with a 1:20 w/v glycerinated-saline whole soybean extract. Sera from six of the seven subjects were tested by RAST assay for the presence of specific IgE antibodies to soybean allergens. All patients had elevated levels of serum IgE antibodies to the crude soybean extract; binding values ranged from 2.3 to 28.1 times that of a negative control serum. Before the oral challenges, all patients demonstrated negative puncture skin tests to three commercially available soybean oils and to olive oil (control). On four separate days, patients were challenged with the individual soybean oils and olive oil in random sequence. At 30-minute intervals, under constant observation, patients ingested 2, 5, and 8 ml of one of the soybean oils or olive oil contained in 1 ml capsules. No untoward reactions were observed with either the commercially available soybean oils or olive oil. Soybean oil ingestion does not appear to pose a risk to soybean-sensitive individuals.

Antibodies, Anti-Idiotypic↗
PubMed1985

Role of serum in stimulation of polymorphonuclear leukocyte, luminol-dependent chemiluminescence by influenza A.

Granulocyte membrane perturbation activates oxidative metabolism with the release of highly reactive species (O2-, H2O2, OH., and 'O2) and emission of light (chemiluminescence (CL)). Using the CL response as a measure of oxidative metabolism, we assayed the effects of influenza A on the granulocyte respiratory burst. Human polymorphonuclear leukocytes (PMNs) were isolated by Ficoll-Hypaque cushioning and dextran sedimentation. The isolated PMNs were incubated with egg-grown influenza A (H3N2) virus, or a medium control, in the presence of 1 microM luminol and fresh autologous serum (10%). No light emission occurred during the incubation of PMNs with the medium control. Influenza A (33 to 50% egg-infective-doses (EID50):1 PMN) stimulated PMN light emission with a maximal response (48,386 +/- 10,764 cpm/10(6) PMN) occurring at 37 degrees CL was dependent on the virus dose with a diminished response (6,041 +/- 3,200 cpm/10(6) PMN) occurring at a lower infectivity of 10 EID50:1 PMN. Chemiluminescence responses were similar with infective and with noninfective virus particles (heat inactivated, 56 degrees C X 2 h). Fresh serum was necessary for the influenza virus to cause a CL response. A significant correlation (p less than 0.01) existed between the level of light emission and the hemagglutination-inhibiting (HI) antibody titer to influenza A of the autologous serum. Virus in the absence of detectable antibody did not stimulate CL. The virus-associated CL was completely inhibited if autologous serum was heated (56 degrees C X 30 min) or if the PMNs were pretreated with cytochalasin B (5 mcg/ml X 5 min). These findings suggest that influenza A-associated PMN CL requires antibody, complement, and phagocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

In vivo and in vitro studies on the use of the guinea pig as a model for virus-provoked airway hyperreactivity.

The parainfluenza 3 (P-3)-infected guinea pig was examined as a model for virus-provoked airway hyperreactivity by measuring changes in airway overflow pressure in response to intravenously (iv) administered histamine. In vitro responses of lung parenchymal strips to several contractile substances were also measured. All studies were conducted 4 days after nasal insufflation with P-3 or P-3 growth medium (control). Increases in airway overflow pressure caused by histamine were enhanced by P-3 infection, and the dose required to produce a standard level of response was decreased (i.e., there was an increase in sensitivity to histamine). Enhancement of in vivo histamine responses caused by P-3 was prevented both by cutting the vagus nerves in the midcervical region and by iv administered hexamethonium, 5 mg/kg. The enhancement was not blocked by 1 mg/kg of atropine given iv, but was blocked by a larger dose 5 mg/kg. The larger dose of atropine significantly antagonized responses to histamine in the P-3-infected state. Increases in airway overflow pressure produced by electrical stimulation of the left vagus and nicotine (1 and 10 mg/kg given iv), both studied after bilateral vagotomy and propranolol, 1 mg/kg given iv, were also enhanced by P-3 infection. Atropine, 1 mg/kg given iv blocked the P-3-induced enhancement of responses to vagus stimulation. Propranolol, 1 mg/kg, and phentolamine, 3 mg/kg, given together iv, produced a doubling of the airway overflow pressure only in P-3-infected animals. Propranolol alone or other receptor antagonists did not produce as marked a change in either group of animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1985

The effect of procaterol treatment on beta-adrenergic bronchodilation and polymorphonuclear leukocyte responsiveness.

Procaterol is a new and effective beta-adrenergic bronchodilator. To determine if procaterol administration could cause tachyphylaxis, airway and leukocyte beta-adrenergic function were monitored in 10 patients with asthma during two 4-wk, double-blind treatment periods, each preceded by a 2-wk beta-agonist washout. Treatment periods were randomized to placebo or procaterol (2 wk, 0.1 mg/day; 2 wk, 0.2 mg/day). At each 7 biweekly evaluations, the patient's cumulative bronchodilator dose-response to inhaled isoproterenol (0.1 to 0.64%) was measured, and venous blood was collected to quantitate, in vitro, the polymorphonuclear leukocyte (PMN) beta-adrenergic receptor's 125Iodo-cyanopindolol (125I-CYP) ligand binding and the PMN cyclic AMP response to isoproterenol and procaterol. Neither the airway nor leukocyte beta-adrenergic characteristics were changed during placebo treatment. Procaterol treatment reduced (p less than 0.05) the maximal 125I-CYP binding to PMN membranes but only during the initial 2 wk at low dosage. The percent PMN cyclic AMP increase to procaterol (10(-5) M) was also significantly (p less than 0.05) less during active treatment (141 +/- 40%) than during washout (256 +/- 24%) or placebo (257 +/- 32%). In contrast, procaterol treatment did not alter the acute isoproterenol bronchodilation response as measured by either the percent improvement in FEV1 or the dose required to produce 50% maximal bronchodilation. The duration of bronchodilation was not measured. Therefore, although procaterol therapy of asthma is associated with decreased PMN beta-adrenergic function, airway smooth muscle function appears not to be altered.

Adult↗
PubMed1985

The precipitation of asthma by upper respiratory infections.

A number of important mechanisms have been identified by which viruses can provoke asthma. From the data available, there does not appear to be one single mechanism available to explain virus-induced asthma. The relationship between viral URIs and asthma is complex and involves many organ systems: airway epithelium, autonomic nervous system control, and the immediate hypersensitivity system. Identifying the effects of respiratory viruses on airway function remains an important undertaking as we try to better understand and control this precipitant of asthma.

Adolescent↗
PubMed1985

Facial edema and eosinophilia. Evidence for eosinophil degranulation.

Two patients had recurrent facial edema and peripheral blood eosinophilia. One patient showed a marked increase in the serum level of the eosinophil granule major basic protein. In both patients, skin biopsy samples showed nonspecific mononuclear cell inflammation with few eosinophils. However, immunofluorescence staining showed extracellular localization of the major basic protein within the dermis, similar to that previously shown in chronic urticaria and the recently described syndrome of episodic angioedema with eosinophilia. These observations provide further evidence that degranulation of eosinophils occurs in the skin and suggest that eosinophil mediators may play a role in the development of cutaneous edema.

Blood Proteins↗
PubMed1985

Comparison of superoxide generation and luminol-dependent chemiluminescence with eosinophils and neutrophils from normal individuals.

Although eosinophilia is found in many allergic and hypersensitivity diseases, the function of the eosinophil is not clearly established. To evaluate and characterize this function, anticoagulated blood from normal subjects was separated into purified populations of both eosinophils and neutrophils by a modified method for Percoll gradients. With this separation procedure, highly purified populations of eosinophils (95.0% +/- 2.1%) and neutrophils (97.2% +/- 0.4%) were obtained. Functional response of these two isolated granulocyte cell types was measured by luminol-dependent chemiluminescence (CL) and superoxide generation to opsonized zymosan and phorbol 12-myristate 13-acetate (PMA). Both the eosinophil and neutrophil peak CL response and superoxide generation to zymosan (1 mg), in the presence of autologous serum (10%), were identical. In contrast, when PMA (10(-4) to 10(0) micrograms/ml) was the stimulant, eosinophil CL was at least twofold greater than the neutrophil light emission (1,595,741 +/- 122,435 cpm/5 X 10(5) cells vs. 765,448 +/- 24,171 cpm/5 X 10(5) cells; n = 6). This same differential in responsiveness was seen in superoxide generation. Thus, under certain conditions the eosinophil's respiratory burst may be greater than that of the neutrophil, and this differential in metabolic activity may contribute directly to the eosinophil's inflammatory potential.

Cell Separation↗
PubMed1985

Beclomethasone dipropionate nasal aerosol spray in allergic rhinitis: a comparison of three delivery systems.

In this 3-way crossover study, the currently marketed beclomethasone dipropionate aerosol canister was sprayed intranasally through three different delivery adapters by 48 adult patients with allergic rhinitis. The adapters were evaluated and compared for force of spray, ease of use, preferred length of nozzle, and effectiveness. While all three were considered effective for symptom relief, there was a clear preference for both of the new longer, snout-like nozzle adapters over the currently available delivery system.

Adult↗
PubMed1984

Influenza A virus enhances the human polymorphonuclear leukocyte chemoluminescence response without effecting inhibition by trifluoperazine.

Influenza A virus has been demonstrated to enhance superoxide generation and chemoluminescence (CL) in human polymorphonuclear leucoytes (PMNs) under in vitro conditions. Although the mechanisms of virus-enhanced neutrophil activity is not established, calmodulin concentrations are known to increase in some virus-transformed cells. In the following experiments, we evaluated the PMN response to the calmodulin-inhibitor trifluoperazine (TFP) after an incubation with influenza A virus. Human PMNs were isolated from whole blood and were incubated with either influenza A virus (at 50% egg-infective dose per 1 leukocyte) or noninfected allantoic fluid. After incubation with influenza virus, the CL response of isolated PMNs to opsonized zymosan particles was measured. The influenza virus-treated PMNs had a mean (+/- SEM, n = 16) increase in light emission of 59.5 +/- 7.7%. TFP, in concentrations of 6 micron, 8 micron, and 10 microM, inhibition of CL was similar in influenza virus and allantoic fluid-treated neutrophils. These data suggest that, although the influenza A virus enhanced the PMN "respiratory burst" to opsonized zymosan particles, it did not alter the cell response to one calmodulin inhibitor, TFP.

Calmodulin↗
PubMed1984

Isoproterenol inhibition of isolated human neutrophil function.

The human PMN can contribute to the inflammatory response. Several neutrophil responses can be inhibited by agonists that increase the cellular levels of cyclic AMP. In the following article, we compared the effects of ISO on lysosomal beta-glucuronidase release, superoxide generation, and CL in isolated human PMNs. ISO inhibited the neutrophil CL response to opsonized zymosan in a dose-dependent fashion with maximal effects at 10(-4)M. ISO inhibition of CL was not enhanced by the addition of theophylline, nor was CL inhibited by the exogenous addition cyclic AMP except at a very high concentration of 10(-3)M. ISO also suppressed beta-glucuronidase release and superoxide generation in neutrophils during an incubation with opsonized zymosan particles. For ISO to inhibit beta-glucuronidase release and superoxide generation, theophylline (5 X 10(-4)M) was necessary. ISO effectively inhibits three neutrophil functions that are capable of causing tissue inflammation. Although ISO suppressed all three neutrophil responses, the inhibitory mechanisms appear to be variable.

Anti-Inflammatory Agents↗
PubMed1984

Flavonoid modulation of human neutrophil function.

Flavonoids are naturally occurring plant compounds that have been demonstrated to possess a variety of anti-inflammatory effects. We studied the effects of flavonoids on three aspects of neutrophil function that are commonly considered to be associated with inflammation: the release of lysosomal enzymes, the chemiluminescence (CL) response, and the production of superoxide anion. Quercetin and eight other flavonoids at a 10(-5)M concentration inhibited the neutrophil CL response to opsonized zymosan particles by approximately 60% or more. In contrast, the release of lysosomal beta-glucuronidase from neutrophils stimulated with opsonized zymosan was only inhibited by two flavonoids, quercetin and chalcone, and only at concentrations of 1.5 X 10(-4)M to 2 X 10(-4)M. Quercetin also inhibited the generation of superoxide anion by neutrophils but to a lesser degree than its effect on CL. The present studies demonstrated that certain flavonoids are not uniformly active in inhibiting neutrophil CL, beta-glucuronidase release, or superoxide generation. The effects of flavonoids on neutrophil functions probably depend on many variables including the response measured, the activating stimulus, and specific flavonoid structural features.

Cyclic AMP↗
PubMed1984

Regulation of the human polymorphonuclear leukocyte inflammatory response by inhibitors of arachidonic acid metabolism.

Perturbation of the neutrophil membrane by opsonized zymosan particles activates the cell's "respiratory burst." Associated with this activation process is the generation of highly reactive oxygen products, including superoxide, and the release of lysosomal enzymes. Membrane activation also stimulates arachidonic acid metabolism and the generation of a wide variety of products through both the lipoxygenase and cyclooxygenase pathways. In isolated human neutrophils, we have evaluated the effects inhibitors of cyclooxygenase and lipoxygenase upon opsonized zymosan stimulated chemiluminescence, superoxide generation, oxygen consumption, and beta-glucuronidase release. Nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase enzyme, suppressed chemiluminescence, superoxide generation, oxygen consumption, and beta-glucuronidase release. Both indomethacin, a cyclooxygenase inhibitor, and 5,8,11,14 - eicosatetraynoic acid (ETYA) an inhibitor of both cyclooxygenase and lipoxygenase, inhibited all tested neutrophil functions. However, when compared to NDGA, indomethacin and ETYA were considerably less potent. Our observations suggest that the lipooxygenase derived metabolites play a predominant regulatory role in these neutrophil inflammatory functions.

Anticoagulants↗
PubMed1984

Cytochalasin B facilitates the inhibition of human polymorphonuclear leukocyte generation of superoxide by verapamil.

Several functions of the human neutrophil are dependent upon extracellular calcium for optimal activation. We studied the calcium dependency of human polymorphonuclear leukocyte (PMN) superoxide generation in response to opsonized zymosan particles and its modulation by the calcium channel antagonist verapamil. PMNs were isolated from anticoagulated blood after Ficoll-Hypaque density centrifugation. The isolated PMNs were incubated with opsonized zymosan particles. The superoxide anion generated was measured by a cytochrome C reduction assay. When PMNs were incubated with opsonized zymosan in a calcium-free buffer, there was 0.45 +/- 0.06 nmol of cytochrome C reduced per 1 X 10(6) PMN per minute. This increased to 0.76 +/- 0.12 nmol per 1 X 10(6) PMN per minute when 0.6 mmol/L Ca++ was present. Moreover, if the PMNs were incubated with cytochalasin B (5 micrograms/ml), the generation of superoxide anion was further enhanced. If the same experiments were conducted in the presence of verapamil, 100 mumol/L, superoxide generation was inhibited by 51.5% +/- 8.4%. For verapamil to inhibit superoxide generation, cytochalasin B was necessary. Our results suggest that verapamil-sensitive calcium channels may exist in human PMNs, and the demonstration of their presence is cytochalasin B-dependent.

Calcium↗
PubMed1983

Pharmacological alteration of antigen-induced contraction of lung parenchymal strips isolated from the actively sensitized guinea pig.

Several drugs, known to influence the action or formation of histamine and SRS-A, were examined for their abilities to alter antigen (ovalbumin)-induced contractions of guinea-pig isolated lung parenchymal strips. Cumulative dose-response effects of ovalbumin were obtained on paired parenchymal strips, one used as control and the other drug treated. When used alone, mepyramine, 10(-6) M, phenoxybenzamine, 3 x 10(-5) M and FPL55712, 10(-5) M, did not alter ovalbumin-induced contractions, 5,8,11,14-eicosatetraynoic acid (ETYA), 10(-4) M, produced a small (2.5-fold) rightward shift of the dose-response curves to ovalbumin and histamine. Indomethacin, 5 x 10(-6) M, produced a small increase in the maximum response to ovalbumin and a small (2-fold) rightward shift of the histamine dose-response curve. The effect of indomethacin on ovalbumin-induced contraction was not seen in the presence of phenoxybenzamine and may therefore be due to an increase in histamine release. Combination of indomethacin with FPL55712 or ETYA did not alter antigen-induced contractions. The effect of ETYA on the histamine dose-response curve was not seen in the presence of indomethacin. Combination of phenoxybenzamine with FPL55712 or ETYA caused a marked reduction of the maximum contractile response to ovalbumin. The effect of phenoxybenzamine and ETYA was not observed in the presence of indomethacin. The results suggest that the ability of ETYA to reduce antigen responses in the absence or presence of phenoxybenzamine as well as histamine-induced contraction is related to inhibition of contractile product(s) of cyclooxygenase metabolism of arachidonic acid.(ABSTRACT TRUNCATED AT 250 WORDS)

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1983

Effect of influenza A virus on leukocyte histamine release.

Viral respiratory infections provoke asthma in many patients. In the following study we examined the effect of an in vitro incubation of influenza A on leukocyte histamine release. After incubation with a live influenza A (H3N2) virus, calcium ionophore A23187 (0.5, 1.0, and 1.5 microgram/ml)-induced leukocyte histamine release (HR) was enhanced (p less than 0.05). This effect was also found with heat- or ether-inactivated virus. Similarly, influenza A-exposed leukocytes had augmented leukocyte HR during subsequent incubation with ragweed AgE. Incubation of the leukocyte suspension with interferon (800 IU/ml) for 24 hr was also associated with enhanced HR to ragweed AgE. In contrast, interferon did not alter the calcium ionophore A23187 HR. Therefore, although interferon may mediate the enhanced leukocyte HR when ragweed AgE is the inciting stimulus, it does not change HR to the calcium ionophore.

Asthma↗
PubMed1983

Exercise-induced anaphylaxis.

Anaphylaxis can pose a life-threatening situation for many patients. A recent report has added exercise to the stimuli which can provoke an anaphylactic reaction. In this report, we review nine cases of anaphylaxis with exercise and the characteristics of this response. These cases represent additional evidence that exercise-induced anaphylaxis is not rare but can be misdiagnosed in some patients.

Adult↗