title: Anti-IgE-induced accumulation of leukocytes, mediators, and albumin in skin chamber fluid from healthy and atopic subjects.
abstract: The aim of this study was to examine potential differences between healthy and atopic subjects with regard to IgE-mediated cutaneous inflammation. For this purpose, we analyzed histamine, tryptase, leukotriene B4, albumin, eosinophils, and total leukocytes in skin chamber fluid after challenge with anti-human IgE. We also measured gross skin reactivity (wheal, flare, and late-phase reactions), circulating IgE, and eosinophils, as well as the state of eosinophil activation. It was found that despite having more circulating IgE, the skin responsiveness of the atopic subjects did not differ significantly from that of the nonatopic subjects with respect to mediator release, albumin extravasation, or total recruitment of leukocytes. Moreover, the sizes of anti-IgE-induced wheal, flare, and late-phase reactions were very similar in the two groups. On the other hand, significant recruitment of eosinophils during the IgE-mediated reaction was more or less restricted to the atopic group. Yet the recruited eosinophils, of which the majority was in an early state of activation before degranulation, did not seem to contribute significantly to the IgE-mediated delayed skin edema. Furthermore, the eosinophil count in anti-IgE chambers of the atopic subjects did not correlate with any of the other parameters monitored. Thus because the anti-IgE-induced recruitment of eosinophils appeared to be unrelated to factors such as the number of peripheral blood eosinophils, the degree of mast cell activation, the intensity of inflammatory skin changes, and the level of circulating IgE, it is apparent that the mechanisms for and pathophysiologic role of IgE-mediated dermal eosinophil accumulation in atopic subjects require further investigation.
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Hospital, Stockholm, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: Raud
authors.forename: G
authors.initials: G
authors.lastname: Halldén
authors.forename: A
authors.initials: A
authors.lastname: Roquet
authors.forename: M
authors.initials: M
authors.lastname: van Hage-Hamsten
authors.forename: U
authors.initials: U
authors.lastname: Alkner
authors.forename: J
authors.initials: J
authors.lastname: Hed
authors.forename: O
authors.initials: O
authors.lastname: Zetterström
authors.forename: S E
authors.initials: SE
authors.lastname: Dahlén
authors.forename: P
authors.initials: P
authors.lastname: Hedqvist
authors.forename: R
authors.initials: R
authors.lastname: Grönneberg
mesh_terms: D000888:Antibodies, Anti-Idiotypic / Q000494:pharmacology*; D002634:Chemotaxis, Leukocyte / Q000276:immunology*; D015194:Diffusion Chambers, Culture; D004804:Eosinophils / Q000276:immunology; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000378:metabolism*; D007073:Immunoglobulin E / Q000276:immunology*; D018836:Inflammation Mediators / Q000378:metabolism*; D012709:Serum Albumin / Q000378:metabolism*; D012867:Skin / Q000276:immunology* / Q000378:metabolism / Q000473:pathology
chemical_list: D000888:Antibodies, Anti-Idiotypic; D018836:Inflammation Mediators; D012709:Serum Albumin; D007073:Immunoglobulin E