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Biomedical subjects

A B Kay

Publications and source records attributed to A B Kay.

At least 361 records · Page 20Linked to original sources
PubMed1981

Chironomid midges as a cause of allergy in the Sudan.

Hypersensitivity to Chironomidae (non-biting midges) has been a problem in the Sudan since about 1927 and appears to be due to increased breeding of a single chironomid species, Cladotanytarsus lewisi (Freeman). Mass emergence of the midges in thought to be related to the larval diet of algae and diatoms, the numbers of which are greatly enhanced by the retention of plant nutrients in lacustrine conditions resulting from interruption to the natural flow of the Nile by the construction of dams. Immunological studies in allergic individuals using an allergen extract prepared from C. lewisi indicate that the concentration of specific immunoglobulin E ("allergic antibody") directed against C. lewisi is raised in patients with established hypersensitivity to the midge but not in control subjects. The concentration of specific IgE is also related to the severity of clinical symptoms. These results indicate that this widespread and important "man made" hypersensitivity in the Sudan has the features of well recognized immediate-type allergy commonly associated with pollens and other air-borne allergens.

Allergens↗
PubMed1981

Mediators of hypersensitivity in the sputum of young, symptomatic cigarette smokers.

We have measured the concentrations of mediators of hypersensitivity in the sputum of twenty-five young, symptomatic cigarette smokers who regularly expectorated and twenty-three matched non-smokers with a respiratory infection. The measurements included sputum and blood eosinophils, IgE, IgG, IgA and IgM and also sputum histamine. We found a significant increase of sputum histamine, and a higher sputum/serum ratio of IgE in smokers when compared to non-smokers. These findings support the view that the bronchial inflammatory response in smokers, as in chronic bronchitis, involves the participation of mediators of hypersensitivity.

Adult↗
PubMed1981

Morphological studies on the killing of schistosomula of Schistosoma mansoni by human eosinophil and neutrophil cationic proteins in vitro.

Purified eosinophil and neutrophil cationic proteins isolated from the lysosomal secretion granules of human granulocytes, evoke characteristic, dose-dependent morphological changes in young schistosomula of S. mansoni. The first sign of damage is seen with in 15-30 min of incubation and involves the formation of surface microvilli and blebs. Subsequently, tegumental evaginations of varying size are developed, but these appear to explode with rapidity, so that lengths of expanded tegumental outer membrane are deposited over the severely damaged surface of the parasite. Both types of granulocyte proteins are able to effect comparable damage at equimolar concentration. Other cationic proteins such as protamine and poly-L-arginine also damage the parasite surface but the pathological changes differ from those induced by the granulocyte proteins and they take longer to develop. In contrast, lysozyme-treated parasites are virtually similar to control schistosomula incubated in medium alone. These findings are discussed in relation to published data concerning the interaction of intact granulocytes with young schistosomula both in vitro and in vivo.

Animals↗
PubMed1981

The effects of an ECF-A and formyl methionyl chemotactic peptides on oxidative metabolism of human eosinophils and neutrophils.

An ECF-A tetrapeptide (Val-Gly-Ser-Glu) and the synthetic bacterial analogue, formyl Met-Leu-Phe (agents previously recognized to be chemotactic and to enhance complement receptors on human eosinophils and neutrophils), were tested for their capacity to evoke a spontaneous burst of light emission (chemiluminescence), and to affect oxygen-consuming reactions induced by contact with serum-treated zymosan (STZ). Superoxide anion (O-2) production by neutrophils induced by STZ was significantly enhanced in both a time- and concentration-dependent fashion by F-Met-Leu-Phe, and to a lesser extent, by F-Met-Met-Phe. The dipeptide F-Met-Phe and unformylated Met-Leu-Phe were inactive. In addition, significant enhancement of eosinophil O-2 generation, by the valyl- ECF-A tetrapeptide was demonstrable and, in addition, this peptide appeared to have an inhibitory effect on neutrophil superoxide anion generation. Eosinophils and neutrophils both produced a burst of chemiluminescence when treated with F-Met-Leu-Phe. With both cell types the magnitude of the responses was similar although with eosinophils peak activity occurred within 60 sec as compared to 2-6 min for neutrophils. No chemiluminescent response was achieved with the valyl- ECF-A tetrapeptide using either cell type. These experiments (1) suggest that ECF-A and formyl methionyl peptides amplify reactions associated with the respiratory burst of eosinophils and neutrophils respectively, and (2) support the view that the generally greater metabolic activity of eosinophils may be related to the special role that this cell may play in the killing of helminthic parasites.

Adult↗
PubMed1981

Inhibition of monocyte complement receptor enhancement by low molecular weight material from human lung cancers.

We have studied the effect of dialysates from lung cancer homogenates to alter both the expression of complement (C3b) receptors per se and also to inhibit leucoattractant-induced enhancement of complement rosettes on monocytes from healthy individuals. Enhancement and enhancement-inhibition by tumour extracts were compared with material derived from normal lung excised from distance from the tumour. There was no significant difference between tumour homogenate (TH) and normal lung homogenate (NLH) in terms of enhancement of complement rosettes per se. In contrast, TH produced a dose- and time-dependent inhibition of leucoattractant-induced enhancement of C3b rosettes which was significantly different from that obtained with NLH. This enhancement-inhibition was observed with four undifferentiated, four squamous and three adenocarcinomas of lung. The degree of enhancement-inhibition was not related to the type of tumour or varying accompanying histological features such as necrosis and the degree of infiltration with inflammatory cells. Following gel filtration on Sephadex G-50 each type of cancer gave a major peak of inhibitory activity which eluted with molecules having an apparent molecular size of approximately 3,000 daltons. A second larger peak (8,000-10,000 daltons) was also detected with extracts from the undifferentiated and adenocarcinomas. These results support previous findings, mainly from experimental animals, indicating that 'anti-macrophage/monocyte principles' are elaborated from certain tumour types.

Carcinoma↗
PubMed1981

Corticosteroid-resistant chronic asthma and monocyte complement receptors.

Monocyte complement receptors (MCR) and enhancement of MCR by a monocyte chemotactic factor (casein) (CRE) were measured in corticosteroid-resistant and corticosteroid-responsive chronic asthmatics. In newly-diagnosed patients who subsequently responded to corticosteroids, the percentage of MCR and CRE was lower after taking oral prednisolone for 7 days and returned to pretreatment values when prednisolone was withdrawn. MCR and CRE in corticosteroid-responsive asthmatics receiving prednisolone were significantly lower than in corticosteroid-resistant asthmatics taking prednisolone. However, there was no significant difference in MCR and CRE between non-responders taking prednisolone and non-responders receiving other forms of therapy. These results suggest that one of the effects of systemic corticosteroids in asthmatics who respond to this form of treatment is a decrease in both MCR and the degree of CRE. Since these changes were not found in corticosteroid-resistant chronic asthmatics such patients may have a defect in the expression and mobilization of complement receptors on the monocyte cell membrane.

Asthma↗
PubMed1981

Histamine receptors on human peripheral blood leucocytes.

Human blood leucocytes were tested for their capacity to bind histamine coupled as a rabbit serum albumin conjugate (H-RSA) to formalized ox red cells. The percentage of rosette-forming target cells was directly related to the concentration of erythrocyte-bound H-RSA. Under optimal experimental conditions the average number of rosettes was 52% for monocytes, 3 for lymphocytes, 25% for neutrophils and 59% for eosinophils. Free histamine partially inhibited rosette formation by blood monocytes in a dose-dependent fashion from 10-3 to 10-5 mol/l, and complete inhibition was achieved by the H-RSA conjugate. In contrast, three amines chemically related to histamine, L-histidine, imidazoleacetic acid and N-acetylhistamine, had no inhibitory effect. The histamine H1 antagonists, mepyramine and chlorpheniramine, and the H1 receptor agonist, 2-(2-aminoethyl)-thiazole, all inhibited rosette formation by blood monocytes in a dose-dependent fashion. However, the H2 receptor antagonists, burimamide and metiamide, and the H2 receptor agonists, Dimaprit and 4-methyl-histamine, were inactive. There was no statistical difference in the percentage of histamine rosettes for monocytes. lymphocytes, neutrophils or eosinophils between atopic and non-atopic individuals.

Humans↗
PubMed1980

H1-receptor dependence of histamine-induced enhancement of human eosinophil C3b rosettes.

The pharmacological specificity of histamine-induced enhancement of human eosinophil C3b rosettes was studied using H1- and H2-receptor agonists and antagonists. The H1 agonist, 2-(2-aminoethyl) thiazole (2-2-AET), enhanced eosinophil C3b rosettes in a comparable fashion to that of histamine, whereas the H2 agonists, 4-methylhistamine and Dimaprit, were without effect. Similarly, rosette enhancement by histamine was inhibited by the H1 antagonists, chlorpheniramine and mepyramine, but not by the H2 antagonists, burimamide and metiamide. These experiments indicate that enhancement of eosinophil C3b rosettes by histamine, a mechanism which might be of importance in the amplification of complement-dependent killing of helminthic larvae, is predominantly H1-receptor-dependent.

Complement C3b↗
PubMed1980

Enhanced expression of human monocyte complement (C3b) receptors by chemoattractants.

The capacity of various leucoattractants to enhance, or unfold, receptors for complement (C3b) on human blood monocytes has been studied. A number of recognized monocyte chemoattractants including casein, supernatants from C. parvum 10390 and from human lymphocytes (cultured either in the presence or absence of phytohaemagglutinin) and the formyl-methionyl peptides, F-Met-Leu-Phe, F-Met-Met-Phe and F-Met-Phe, increased the percentage of monocytes which formed rosettes with IgM-sensitized sheep erythrocytes coated with complement. Comparable results were achieved irrespective of whether purified components of whole serum was used as a source of complement. In contrast, there was no significant increase in EAG (Fc) rosettes with those doses of casein which gave enhancement of C3b receptors. A small degree of complement receptor enhancement was observed with histamine but the unformylated peptides, Met-Leu-Phe and Met-Met-Phe, were without apparent effect. Maximal receptor enhancement was obtained at 30 min but when the leucoattractant was removed, enhancement was reversible, returning to normal values in approximately 120 min. Monocyte complement receptor enhancement increased with temperatures between 0 degrees C and 37 degrees C. These data (1) confirm and extend our previous findings on leucoattractant-induced enhancement of complement receptors on human monocytes; (2) indicate that the phenomenon may have potential as a clinical test for monocyte function both in health and disease.

Caseins↗
PubMed1980

Histamine increases histidine uptake by basophils.

Histamine, at high concentrations, enhanced the uptake of isotopic histidine by guinea-pig basophils. The effect was partially reversed by H1-, but not H2-, histamine receptor antagonists. These data suggest that histamine has a bioregulatory role in its own synthesis.

Animals↗
PubMed1980

Widespread IgE-mediated hypersensitivity in the Sudan to the 'green nimitti' midge, Cladotanytarsus lewisi (Diptera: Chironomidae) II. Identification of a major allergen.

A major allergen has been identified in an aqueous extract of the 'green nimitti' midge, Cladotanytarsus lewisi (Diptera: Chironomidae). Following chromatography on Sephadex G-100 allergenic activity, as assessed by skin ('prick') testing, eluted as two closely related peaks (pools I and II) at about 50% bed volume. When these pools were applied separately to columns of CM-cellulose, activity in each eluted with 0 . 05 M NaCl. Isoelectric focusing of the unfractionated allergen gave a single peak of activity at pI 4 . 3. By SDS--PAGE, biological activity in the whole 'green nimitti' extract and the material eluting from both pools I and II of the Sephadex G-100 column migrated to the same positions and were associated with a molecular size of 15,000--20,000 daltons. Skin test reactivity of the unfractionated material and the Sephadex G-100 pool I and II eluates were all destroyed following incubation with trypsin, chymotrypsin, thermolysin and neuraminidase. These experiments indicate that a major allergen derived from the 'green nimitti' midge, a cause of widespread and severe immediate-type allergy in the Sudan, is an acidic glycoprotein of 15,000--20,000 molecular weight.

Allergens↗