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Biomedical subjects

S I Wasserman

Publications and source records attributed to S I Wasserman.

At least 109 records · Page 6Linked to original sources
PubMed1977

Cold urticaria. Recognition and characterization of a neutrophil chemotactic factor which appears in serum during experimental cold challenge.

Sera were obtained from the venous effluents of cold-challenged arms of patients with idiopathic cold urticaria without plasma or serum cryoproteins; these sera exhibited increased neutrophil chemotactic activity without alterations of the complement system. A two- to fourfold augmentation of the base-line neutrophil chemotactic activity of serum from the immersed extremity began within 1 min, peaked at 2 min, and returned to base-line levels within 15 min, whereas there was no change in the serum chemotactic activity in the control arm. The augmented chemotactic activity in the serum specimens from the challenged arm of each patient appeared in a high molecular-weight region, as assessed by the difference in activity recovered after Sephadex G-200 gel filtration of the paired lesional and control specimens. Sequential purification of this high molecular-weight activity by anion- and cation-exchange chromatography revealed a single peak of activity at both steps. The partially purified material continued to exhibit a high molecular weight, being excluded on Sepharose 4B, and had a neutral isoelectric point. The partially purified material showed a preferential chemotactic activity for neutrophilic polymorphonuclear leukocytes, required a gradient for expression of this function, and exhibited a capacity to deactivate this cell type. This active principle, termed high molecular-weight neutrophil chemotactic factor, exhibited a time-course of release that could be superimposed upon that of histamine and the low molecular-weight eosinophil chemotactic factor and may represent another mast cell-derived mediator.

Chemotaxis, Leukocyte↗
PubMed1976

Cold urticaria: release into the circulation of histamine and eosinophil chemotactic factor of anaphylaxis during cold challenge.

Patients with idiopathic acquired cold-induced urticaria were evaluated for the release of the preformed mast-cell mediators of immediate-type hypersensitivity during a study in which one arm was immersed in ice water while the other arm remained as a control. Blood specimens were obtained from each arm serially over a one-hour interval, and serum speciments were assessed for histamine, eosinophil chemotactic factor of anaphylaxis, and complement components. Levels of histamine and eosinophil chemotactic factor rose in the arm subjected to cold immersion for three minutes, with peak values occurring between two and five minutes and returning to base line by 30 minutes. No changes occurred in the control arm or in the immersed arm of normal subjects. Assessment of the classical and alternative complement pathways showed no abnormalities. This initial observation of release of eosinophil chemotactic factor of anaphylaxis in vivo along with histamine assigns the mast cell a central role in cold urticaria.

Anaphylaxis↗
PubMed1976

Arylsulfatase B of human lung. Isolation, characterization, and interaction with slow-reacting substance of anaphylaxis.

Arylsulfatase B was separated from arylsulfatase A in extracts of human lung tissue by anion exchange chromatography and further purified by gel filtration and cation exchange chromatography. Arylsulfatase B of human lung was similar to that enzyme in other tissues and species, exhibiting an apparent mol wt of approximately 60,000, a pH optimum for cleavage of 4-nitrocatechol sulfate (pNCS) of 5.5-6.0, and a sensitivity to inhibition by phosphate ions and especially pyrophosphate in the presence of NaCl. Human lung arylsulfatase B inactivated slow-reacting substance of anaphylaxix (SRS-A) in a linear time-dependent reaction in which the rate was determined by the enzyme-to-substrate ratio. Cleavage of pNCS by human lung arylsulfatase B was competitively suppressed by SRS-A. The finding that human lung tissue contains predominately arylsulfatase B discloses a potential regulatory mechanism for inactivation of SRS-A at or near the site of its generation.

Chondro-4-Sulfatase↗
PubMed1976

Release of chemical mediators from partially purified human lung mast cells.

Human lung mast cells dispersed by enzymatic digestion of human lung fragments were concentrated to greater than 50% purity by sedimentation in isopycnic and velocity gradients. The dispersed lung mast cells had a characteristic ultrasturctural appearance including granules with a scroll or reticular structural appearance including granules with a scroll or reticular structure surrounded by perigranular membranes. Histamine and preformed eosinophilotactic activity sedimented with mast cells on isopycnic gradients, and mast cells and these mediators were separated from the bulk of the other lung cells after velocity gradient sedimentation. The histamine content of isolated lung mast cells was calculated to range from 1.0 to 5.5 pg/cell. The quantity of SRS-A generated with anti-IgE or specific antigen was relatively limited but confined to the mast cell-rich fractions and associated with release of histamine and eosinophilotactic activity.

Centrifugation, Isopycnic↗
PubMed1975

Chemotactic deactivation of human eosinophils by the eosinophil chemotactic factor of anaphylaxis (38527).

Purified human eosinophils demonstrate diminished chemotactic responsiveness (deactivation) after incubation with the eosinophil chemotactic factor of anaphylaxis (ECF-A). The deactivation is rapid and selective in that ECF-A deactivated human eosinophils more markedly than neutrophilic or mononuclear leukocytes. The eosinophil can also be deactivated by C5a which is eosinophilotactic, and there is cross deactivation between C5a and ECF-A. Deactivation may be an important physiologic control mechanism enabling the eosinophil to remain at sites of ECF-A release in order to manifest its regulatory functions in immediate hypersensitivity reactions.

Anaphylaxis↗
PubMed1975

Eosinophil polymorphonuclear leukocyte function in immediate hypersensitivity.

An eosinophil chemotactic factor of anaphylaxis (ECF-A), released along with other chemical mediators of immediate hypersensitivity from sensitized mast cells that have been challenged with specific antigen, is capable of selectively attracting eosinophils. The rate and magnitude of tissue eosinophil influx may be enhanced by ascorbate and inhibited by the neutrophil immobilizing factor (NIF). Eosinophils may then exercise a local regulatory function. Phagocytosis or the action of ECF-A at high concentrations causes eosinophils to release arylsulfatase, which inactivates slow reacting substance of anaphylaxis (SRS-A). Additional possible functions of eosinophils may follow from their content of factors that inhibit histamine release or its mediator function, and the high levels of intracellular plasminogen and phospholipase B. Thus, the unique enzymes and factors released from eosinophils may form the basis of their role in immediate and subacute hypersensitivity reactions.

Anaphylaxis↗
PubMed1975

Inactivation of slow reacting substance of anaphylaxis by human eosinophil arylsulfatase.

Arylsulfatase preferentially present in the human eosinophil as compared to other leukocytes was isolated by sequential gel filtration and cation exchange chromatography. The apparent molecular weight of 60,000, the preferential cleavage of 4-nitrocatechol sulfate (PNCS) over p-acetyl-benzenesulfonic acid (PABS), inhibition by phosphate ions and pH optimum of 5.7 are characteristics of a type II B arylsulfatase. Eosinophil arylsulfatase inactivated purified human slow reacting substance of anaphylaxis (SRS-A) in a time-dependent reaction with the rate dependent upon the enzyme/substrate ratio. That SRS-A inactivation was the result of intrinsic arylsulfatase activity was indicated by association of PNCS cleavage and SRS-A inactivating activity during chromatography, the similar pH optimum for cleavage of both substrates and the capacity of SRS-A to inhibit PNCS cleavage by arylsulfatase. The finding that eosinophil arylsulfatase inactivates SRS-A suggests that eosinophil ingress into the site of an immediate hypersensitivity reaction in response to ECF-A could represent a regulatory function.

Centrifugation, Density Gradient↗
PubMed1975

The release of four mediators of immediate hypersensitivity from human leukemic basophils.

The availability of a patient with basophilic leukemia manifesting 75 to 90% mature basophils permitted the use of a cell concentration sufficient to generate and release mediators upon interaction with a calcium ionophore in quantities adequate for their physiocochemical characterization. The mediators were defined in terms of their physicochemical characteristics: slow reacting substance of anaphylaxis (SRS-A) by purification through silicic acid chromatography and inactivation by arylsulfatase; eosinophil chemotactic factor of anaphylaxis (ECF-A) by its gel filtration through Sephadex G-25 and inactivation by subtilisin and not trypsin; and platelet-activating factor (PAF) by its inherent binding to albumin. Both ECF-A and histamine were present in their preformed state, and for histamine it was possible to establish that the concentration per cell was comparable to that of normal human basophils. Dibutyryl cyclic AMP suppressed release of histamine and SRS-A, indicating that their availability was under a control similar to that observed with normal cells subjected to immunologic activation. The demonstration that a suspension of leukemic human basophils contained the preformed mediators, histamine and ECF-A, and generated SRS-A and PAF for release along with histamine and ECF-A, after activation with a calcium ionophore, establishes that a single cell type can serve as a source of the four recognized mediators of immediate-type hypersensitivity.

Aged↗
PubMed1974

Formation of slow-reacting substance of anaphylaxis in human lung tissue and cells before release.

The capacity to extract slow-reacting substance of anaphylaxis (SRS-A) from human lung tissue or cells after immunologic activation, together with the measurement of SRS-A in both the extract and the surrounding fluid, permits study of total SRS-A generation. That the material extracted is SRS-A was established by both differential bioassay and purification. SRS-A accumulation was entirely intracellular after limited IgE-dependent direct or reversed anaphylactic activation. Intracellular accumulation also generally preceded release, with generation of SRS-A continuing well beyond a plateau in the cellular SRS-A level and the release of preformed mediators. The quantity of SRS-A generated after immunologic activation was modulated by the introduction of exogenous cyclic nucleotides, revealing a site of cyclic nucleotide action distinct from that on mediator release. The capacity to determine not only the release of preformed mediators but also the generation of a newly formed mediator, the sum of SRS-A in cells and supernate, adds an additional dimension to the analysis of the cellular events of immediate hypersensitivity.

Anaphylaxis↗
PubMed1974

Enhancement of random migration and chemotactic response of human leukocytes by ascorbic acid.

Incubation of human leukocytes with ascorbic acid at neutral pH and at concentrations 10-50 times that of normal blood levels augmented both the in vitro random migration and chemotaxis of the cells by 100-300% without influencing their phagocytic capacity. Enhancement of mobility by ascorbate was evident for isolated neutrophils, eosinophils, and mono-nuclear leukocytes and was independent of the specific chemotactic stimulus. Stimulation by ascorbate of the hexose monophosphate shunt of adherent neutrophils and augmentation by ascorbate of neutrophil mobility had comparable dose-response relationships, could be reversed by washing the cells, and were both suppressed by preincubation of the neutrophils with 6-aminonicotinamide, but not with the neutrophil-immobilizing factor. Glutathione, the proposed intermediate for ascorbate action, similarly stimulated hexose monophosphate shunt activity and enhanced migration. The enhancement in vitro of leukocyte mobility by ascorbate at concentrations found in some normal tissues, therefore, appears to be dependent upon stimulation of the leukocyte hexose monophosphate shunt.

Ascorbic Acid↗
PubMedDate not supplied

Histamine-induced middle ear effusion and mucosal histopathology in the guinea pig.

It has been suggested that immune responses and resultant generation or release of inflammatory mediators play a role in otitis media with effusion (OME). To explore the potential of one such mediator to contribute to OME, the effects of histamine injected into the middle ear cavity were examined. Injection of histamine into the guinea pig middle ear was found to produce dilation and endothelial disjunction in capillaries, leading to striking mucosal edema and effusion which persisted for at least several hours. This response could be partially blocked by pretreatment with either H1 or H2 antihistamines. It is suggested that histamine released during immune responses in the middle ear may contribute to the formation of effusion and submucosal edema as observed in OME.

Animals↗