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Biomedical subjects

R Moqbel

Publications and source records attributed to R Moqbel.

125 records · Page 7Linked to original sources
PubMed1985

Enhancement of human neutrophil complement receptors: a comparison of the rosette technique with the uptake of radio-labelled anti-CR1 monoclonal antibody.

We have compared the rosette technique (using C3b-coated red cells) with the uptake of a 125I F(ab')2 anti-complement receptor type 1 (CR1) monoclonal antibody (E11) for studying the phenomenon of chemotactic factor (fMLP)-induced complement receptor enhancement (CRE) on human neutrophils. With both methods the dose responses of fMLP were similar with maximal CRE being observed at 10(-7) moles 1(-1). Conversely, the time course of CRE and the effects of disodium cromoglycate (DSCG) on inhibition of enhancement were discrepant. Maximal CRE with the rosette method was observed at 30 min, whereas increased uptake of anti-CR1 had still not reached a plateau after 1 h. DSCG inhibited fMLP-induced CRE, as assessed by the rosette technique, whereas this agent had no effect on increased binding of radio-labelled anti-CR1 antibody. These results suggest that in CRE the increased adherence of C3b-coated red cells to fMLP-stimulated neutrophils, as measured by the rosette technique, is not dependent exclusively on the increased numbers of CR1.

Antibodies, Monoclonal↗
PubMed1985

Enhancement of human eosinophil- and neutrophil-mediated killing of schistosomula of Schistosoma mansoni by reversed type (IgE-mediated) anaphylaxis, in vitro.

Using human peripheral blood leucocytes we have developed a model for studying the effect of in vitro anaphylaxis on granulocyte-mediated killing of helminthic larvae (schistosomula (Sch) of Schistosoma mansoni). Leucocytes were incubated with either an F(ab')2 rabbit anti-human IgE (alpha E) or a control F(ab')2 prepared from non-specific rabbit IgG (alpha Ec). A time-dependent enhancement of eosinophil- and neutrophil-mediated complement (C) or antibody- (Ab) dependent killing of Sch was observed following incubation with alpha E, but not alpha Ec. Optimal enhancement of granulocyte killing was dependent on the concentration of alpha E, pre-incubation of granulocytes with alpha E prior to addition to C coated Sch, as well as the granulocyte: Sch ratio. Baseline killing of Ab and/or C coated Sch by eosinophil rich cells was significantly greater than neutrophil rich suspensions and both were proportionally increased following incubation with alpha E. Enhanced eosinophil and neutrophil killing by alpha E required the presence of mononuclear cells containing basophils, whereas there was no difference in the killing of C or Ab coated Sch when eosinophils or neutrophils alone were incubated with alpha E or alpha Ec. This IgE and leucocyte-dependent model might facilitate the isolation and identification of the pharmacological mediator(s) of hypersensitivity which enhance eosinophil or neutrophil killing of appropriately opsonized helminthic larvae.

Anaphylaxis↗
PubMed1984

Human granulocyte/pollen-binding protein. Recognition and identification as transferrin.

Normal human serum was found to contain a heat-stable protein which promoted the binding of granulocytes to timothy grass pollen (granulocyte/pollen-binding protein [GPBP]). GPBP was purified by gel filtration, anion exchange, and affinity chromatography. Virtually all of the granulocyte/pollen-binding activity was associated with a beta-1-protein having a molecular mass of approximately 77,000 D and an isoelectric point of between 5.5 and 6.1. By immunoelectrophoresis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the protein was identified as transferrin. Monospecific antisera raised against either GPBP or transferrin removed biological activity from GPBP preparations, and GPBP and transferrin gave lines of identity with these two antisera. The apparent heterogeneity in the molecular size and charge of GPBP observed during progressive purification was minimal when GPBP was saturated with ferric ions before the separation procedures. These experiments indicate that granulocyte/pollen binding is a hitherto unrecognized property of transferrin which appears to be unrelated to iron transport and raises the possibility that transferrin might have a physiological role in the removal of certain organic matter.

Carrier Proteins↗
PubMed1983

Enhancement of neutrophil- and eosinophil-mediated complement-dependent killing of schistosomula of Schistosoma mansoni in vitro by leukotriene B4.

We have studied the ability of leukotrienes and other lipoxygenase products of arachidonic acid (AA) to influence complement-dependent killing of schistosomula of Schistosoma mansoni in vitro by human neutrophils or eosinophils. These lipid mediators, which included LTB4, LTC4, LTD4, 5-HETE and 5-HPETE, had no apparent effect, by themselves, on schistosomular motility or viability. However, in the presence of granulocytes and fresh serum (as a source of complement) LTB4 (but not LTC4, LTD4, 5-HETE or 5-HPETE) enhanced neutrophil- and (to a much lesser extent) eosinophil mediated, complement-dependent killing. These effects varied with the concentration of LTB4, the dilution of complement and time of incubation. The percentage of LTB4-induced enhancement obtained with neutrophils was greater than that observed with eosinophils (although the latter were obtained from patients with helminthic parasitic disease). The synthetic bacterial analogue f-Met-Leu-Phe, also known to amplify complement associated granulocyte events, was comparable to LTB4 in its ability to enhance neutrophil- and eosinophil-mediated, complement-dependent killing of schistosomula. These results indicate that LTB4, which is released in mast cell associated reactions and promotes cell locomotion and enhancement of complement receptors in vitro, increases neutrophil- and eosinophil-mediated, complement-dependent damage of schistosomula, possibly through enhancement of C3b receptors and that this may be an important amplification mechanism in IgE related immunity to migrating helminthic larvae.

Arachidonic Acids↗
PubMed1981

Immunity to Strongyloides ratti in rats. 1. Adoptive transfer with mesenteric lymph node cells.

Adoptive transfer of immunity against the enteral phase of Strongyloides ratti was monitored using four parameters; namely, number of worms recovered, position occupied in the host's small intestine, worm length and fecundity. When immune mesenteric lymph node cells (IMLNC) were transferred from donors infected for 20, 26 or 32 days into recipients infected for 3 days, a marked acceleration of worm expulsion was evident by day 16 post-infection (p.i.). IMLNC from day-16 p.i. donors did not transfer expulsion. In an experiment in which recipients were given 2 x 10(8) or 1 x 10(8) IMLNC from donors infected for 26 days, accelerated worm expulsion occurred only with the higher inoculum, although manifestations of direct worm immunity, i.e. altered position and reduced length and fecundity, were evident in both cases. Transfer of IMLNC appeared to have no effect upon worm establishment; when cells were transferred on the day of infection a period of 16 days was necessary to effect both direct anti-worm immunity and expulsion, although the former was evident on day 14 p.i. However, when IMLNC were transferred to rats already infected for 6 days, a very significant reduction of their worm burden was apparent 10 days after IMLNC transfer.

Animals↗
PubMed1978

Strongyloides ratti: the effect of betamethasone on the course of infection in rats.

Rats were treated with betamethasone at different stages of infection with Strongyloides ratti. Treatment caused a diminution in the number of adult worms recovered but this residual population was not expelled as were worms from untreated rats. If treatment was started after expulsion had already begun adult worm numbers increased--suggesting that autoinfection occurred. Treatment throughout a primary infection prevented the development of an immune response which expelled, or killed, a challenge infection. Treatment, just before and just after challenge, prevented the expulsion of the challenge infection. Worm expulsion up to day 35 was prevented by treating rats with betamethasone 4, 6, 8 and 10 days after infection.

Animals↗
PubMedDate not supplied

Activated human eosinophils generate SRS-A leukotrienes following IgG-dependent stimulation.

Eosinophils, a class of granular leukocytes, are prominent in many inflammatory processes, particularly in asthma, certain allergic diseases and during infections with helminthic parasites. Following incubation with the Ca ionophore A23187 (refs 1-4) (a non-physiological agent which circumvents membrane calcium-gating mechanisms), eosinophils generate large amounts of sulphidopeptide leukotrienes, potent inducers of smooth muscle constriction and mucus production. These are now known to represent the activity previously termed 'slow-reacting substance of anaphylaxis' (SRS-A) but attempts to identify a physiological stimulus for SRS-A production by eosinophils have so far been unsuccessful. The cells contain recognized receptors for IgG (Fc) and it is known that they adhere to, and can be activated by, contact with the surface of large organisms such as helminthic larvae. We show here that eosinophils, particularly when activated, produce sulphidopeptide leukotrienes after contact with large particles coated with IgG.

Eosinophilia↗
PubMedDate not supplied

Leukotriene receptor antagonists in the treatment of asthma: implications for eosinophilic inflammation.

Recent advances in the treatment and management of asthma have suggested that leukotriene (LT) receptor antagonists may be very beneficial as a second generation therapy with steroid-sparing properties and negligible side effects. These agents have shown interesting effects on peripheral blood and sputum eosinophils. A major contributor to the damage in the airway of asthmatic patients is the eosinophil, which, upon activation, releases a battery of granule-associated cytotoxic, cationic proteins, including the major basic protein and eosinophil peroxidase, and membrane-derived de novo-synthesized bioactive lipid mediators, including LTC4, LTD4 and LTE4, as well as PAF (please spell out). These products have deleterious effects on the airway tissue including mucosal and smooth muscle layers. Accumulating evidence suggests that these agents may also influence the accumulation and maintenance of eosinophilic responses at the site of inflammation. This article reviews the possible anti-inflammatory mode of action of these therapies. It also discusses where there may be a gap in the knowledge regarding the potential direct and indirect effects of LT modifiers on eosinophil function and recruitment.

Asthma↗
PubMedDate not supplied

Effects of interferon-gamma on mobilization and release of eosinophil-derived RANTES.

Eosinophils synthesize and release a number of cytokines and chemokines, including RANTES, a potent chemoattractant particularly for memory T cells and eosinophils. Long-term (>12 h) incubation with interferon-gamma (IFN-gamma) has been shown to activate eosinophils and induce expression of membrane receptors. We hypothesized that IFN-gamma mobilizes intracellular RANTES in eosinophils in advance of mediator release. Highly purified peripheral blood eosinophils were obtained from asthmatics and stimulated with IFN-gamma at 500 U/ml for time course analysis up to 2h. By specific ELISA, RANTES was detected in supernatants (80+/-15 pg per 2x10(6) cells) following 120min of stimulation. Immunoreactive RANTES in resting cells (5x10(7) eosinophils) was detected in two intracellular compartments in studies of subcellular fractionation by density gradient centrifugation. After 10 min IFN-gamma stimulation, RANTES immunoreactivity was confined to crystalloid granules. RANTES was redistributed from secretory granules to light-membrane fractions after 60 min of IFN-gamma incubation. Our data suggest that rapid mobilization and release of RANTES occurs from stimulated eosinophils. These findings may have important implications for the role of IFN-gamma in activating human eosinophils, particularly in severe chronic asthma or viral exacerbation of asthmatic inflammation, where this cytokine may play a role.

Cells, Cultured↗