Anaphylactic relase of a basophil kallikrein-like activity. II. A mediator of immediate hypersensitivity reactions.

Newball, Harold H.; Talamo, Richard C.; Lichtenstein, Lawrence M.

doi:10.1172/jci109484

Cited by 36 publications

(8 citation statements)

References 23 publications

(19 reference statements)

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“…With similar amounts of histamine release induced by antigen or anti-IgE, there would have been detectable SRS (18). Three experiments were carried out to see whether another preformed mediator, ptoluene sulfonyl-L-arginine (TAMe) esterase, was released (19,20). In each case, the dose-response curves for histamine and esterase release were similar in shape, although, as previously reported, there was no quantitative relationship between the two (data not shown).…”

Section: Resultsmentioning

confidence: 65%

Hyperosmolar Triggering of Histamine Release from Human Basophils

Findlay¹,

Dvorak²,

Kagey‐Sobotka³

et al. 1981

J. Clin. Invest.

139

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A B S T R A C T Idiopathic reactions occurring during the infusion of hyperosmolar solutions, such as radiocontrast dyes, cause a significant number ofdeaths each year. These reactions are similar to those which follow mediator release during allergen-induced anaphylaxis. In attempting to explain these nonimmunologic reactions, we examined the direct effect of hyperosmolarity on normal human basophils with emphasis on release induced by mannitol.The cells of all donors released histamine in vitro in response to hyperosmolar (0.2-0.7 M) solutions of a number ofsolutes including mannitol. That this was not a toxic Etocess was supported by a number of criteria, including inhibition of release by excess stimulus at 370C and a lack of release at 4°C. Furthermore, electron microscopic studies revealed that hyperosmolar stimulation did not disrupt the cell membrane or lead to any signs of cytotoxicity. In contrast to antigen-stimulated release, where granules fuse only with the cell membrane, granules in mannitol-stimulated cells, in addition to fusing with the cell membrane, may also be extruded into a common intracellular sac before exteriorization.Characteristics similar to antigen-induced histamine release included the time-course for release, inhibition by drugs that modify phospholipid metabolism, p-bromophenacyl bromide, and eicbsa-5,8, 11,14-tetraynoic acid, and augmentation of release by deuterium oxide (D20). The release process differed from antigen-induced release by a number of criteria, including independence from immunoglobulin (Ig)Erelated mechanisms, insensitivity to agonists that ele-

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Section: Resultsmentioning

confidence: 65%

Hyperosmolar Triggering of Histamine Release from Human Basophils

Findlay¹,

Dvorak²,

Kagey‐Sobotka³

et al. 1981

J. Clin. Invest.

139

View full text Add to dashboard Cite

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“…We earlier suggested that certain chemical mediators, derived from basophils and mast cells, may participate not only in immediate-type inflammatory events, but also in important aspects of the entire inflammatory process (33)(34)(35)(36). Other reports suggest the participation of basophils and/or mast cells in subacute or chronic phases of inflammation.…”

Section: Lung Prekallikrein Activatormentioning

confidence: 99%

“…These reports show deposition of fibrin in and around inflammatory lesions, such as those of cutaneous basophil hypersensitivity (37)(38)(39)(40). It is possible that basophils and mast cells, through the release of LPKA, the HF activator (13,35), or the kininogenase (13,33,34) may activate the HF-dependent systems, and thus participate in inflammatory processes.…”

Section: Lung Prekallikrein Activatormentioning

confidence: 99%

Anaphylactic release of a prekallikrein activator from human lung in vitro.

Meier¹,

Kaplan²,

Lichtenstein³

et al. 1983

J. Clin. Invest.

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A B S T R A C T We have demonstrated the in vitro IgEmediated release of a prekallikrein activator from human lung. The lung prekallikrein activator was partially purified by sequential chromatography on sulfopropyl-Sephadex, DEAE-Sephacel, and Sepharose 6B. Purified human prekallikrein was converted to its active form (kallikrein) by the lung protease. The generated kallikrein was shown to be biologically active; that is, it generates bradykinin from purified human high-molecular weight kininogen and also cleaves benzoyl-propyl-phenyl-arginyl-p-nitroanilide, a known synthetic substrate of kallikrein. The lung prekallikrein activator differs from the known physiologic activators of prekallikrein (the activated forms of Hageman factor) with respect to: (a) size (it has a mol wt of -175,000); (b) synthetic substrate specificity (Dpropyl/phenyl/arginyl-p-nitroanilide is a substrate for the activated forms of Hageman factor, but not the lung protease); (c) antigenic specificity (an anti-Hageman factor immunoadsorbent column did not remove significant amounts of the lung protease, while it removed most of the activity of activated Hageman factor fragments); and (d) inhibition profile (the lung proteases was not inhibited by corn trypsin inhibitor). This prekallikrein activator provides a physiologic mechanism by which prekallikrein can be directly activated during IgE-mediated reactions of the lung. While the role of this lung prekallikrein activator in immediate hypersensitivity reactions and in other inflammatory processes is not clear, it does represent a

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“…Thus, metabolic inhibitors such as 2-deoxyglucose will inhibit the release of mediators from mast cells and basophils. 8 One of the most interesting recent observations with respect to the release of several chemical mediators from mast cells and basophils has to do with the role of arachidonic acid metabolism in the release process. With respect to histamine release, it has been shown that eicosatetraenoic acid (ETYA), which blocks both the lipoxygenase and the cyclooxygenase pathways of arachidonic acid metabolism completely inhibits the release of histamine.…”

Section: Modulation Of Mediator Releasementioning

confidence: 99%