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Research Article Free access | 10.1172/JCI114047

Cutaneous late-phase response to allergen. Mediator release and inflammatory cell infiltration.

E N Charlesworth, A F Hood, N A Soter, A Kagey-Sobotka, P S Norman, and L M Lichtenstein

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

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Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

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Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

Find articles by Soter, N. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

Find articles by Kagey-Sobotka, A. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

Find articles by Norman, P. in: PubMed | Google Scholar

Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21239, USA.

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Published May 1, 1989 - More info

Published in Volume 83, Issue 5 on May 1, 1989
J Clin Invest. 1989;83(5):1519–1526. https://doi.org/10.1172/JCI114047.
© 1989 The American Society for Clinical Investigation
Published May 1, 1989 - Version history
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Abstract

To better define the inflammatory infiltrates and kinetics of mediator release during the cutaneous late-phase reaction (LPR), we examined skin biopsies at 8 h, and skin chamber cell counts and mediator release for 12 h after antigen challenge. Compared with the control sites, the antigen-stimulated biopsy sites contained 14 times as many basophils (P less than 0.01) and six times as many eosinophils (P less than 0.001) with one to two fold more mononuclear cells (P less than 0.03) and neutrophils (P less than or equal to 0.01). Similar changes were found in the skin chambers. Although there were neutrophils in the control chamber, they were only twice as numerous in the antigen challenged site (P less than 0.01). Eosinophils were 35-fold (P less than or equal to 0.03) more prevalent in the antigen chamber than the control chamber for hours 8-12 and basophils were noted starting in the eighth hour and were 20-fold (P less than or equal to 0.03) more concentrated in the antigen chamber during the next 4 h. The mononuclear cells were not significantly different between antigen and control blisters. With respect to inflammatory mediators, there was an initial peak of histamine (13.2 +/- 2.9 ng/ml) in the blister fluid at 1 h. The level then fell to approximately 2 ng/ml, followed by a secondary rise starting at the eighth hour and increasing to 9.8 +/- 2.8 ng/ml by the twelfth hour. This secondary increase in histamine correlated significantly (r = 0.81, P less than 0.05) with the observed influx of basophils. PGD2 in the blister fluid rose to 371+/-25 pg/ml during the first 4 h and then slowly decreased to half this level during the last 4 h. Thus, the cutaneous LPR has been shown to manifest a secondary increase in histamine levels and a markedly specific increase in eosinophils and basophils with mediator release apparently being derived from the latter cells.

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