TY - JOUR
T1 - Interleukin-1 is released at sites of human cutaneous allergic reactions
AU - Bochner, Bruce S.
AU - Charlesworth, Ernest N.
AU - Lichtenstein, Lawrence M.
AU - Derse, Claudia P.
AU - Gillis, Steven
AU - Dinarello, Charles A.
AU - Schleimer, Robert P.
N1 - Funding Information:
From the *Department of Medicine, Division of Clinical Immu-nology, The Johns Hopkins Asthma and Allergy Center, Balti-more, Md., ***Immunex Corp., Seattle, Wash., and ****Tufts University School of Medicine, New England Medical Center, Boston, Mass. Supported by National Institutes of Health Grants AI07290, AI08270, AM31891, and A120136. The opinions expressed are those of the authors and not necessarily those of the Department of Defense or the United States Air Force. Received for publication Feb. 5, 1990. Revised May 16, 1990. Accepted for publication June 29, 1990. Reprint requests: Bruce S. Bochner, MD, The Johns Hopkins Asthma and Allergy Center, Clinical Immunology Unit, Office 3, 301 Baysview Blvd., Baltimore, MD 21224. Dr. Lawrence M. Lichtenstein is a recipient of a Pfizer Biomedical Award. Dr. Bruce S. Bochner is supported in part by a New Investigator Award from the American Lung Association. **Current address: Allergy Department, Wilford Hall United States Air Force Medical Center, Lackland Air Force Base, San An-tonio, Texas. Dr. Charlesworth is a Colonel in the United States Air Force Medical Corps. 1/1/23570 Experimental allergen-challenge reactions in the skin and airways of humans consist of an acute phase that typically subsides within 60 minutes and is often followed in 3 to 12 hours by the development of an intense inflammatory reaction termed the late phase.1 Although the acute response is largely mast cell mediated, the late-phase response is believed to be dependent on the local accumulation and activation of leukocytes, including neutrophils, eosinophils, and basophils. 2-4 This delayed response is of great interest since it more closely resembles the clinical manifestations of chronic allergic diseases .4 To study the late-phase response in greater detail, a variety of antigen-challenge models have been devised, permitting analysis of the pattern of mediator release and cell accumulation during these reactions in vivo. Allergen provocation results in elevated levels of histamine during the acute and late phases in both the nasal and skin-chamber antigen-challenge models. 57 Although acute increases in mast cell-derived tryptase and PGD2 levels are observed, there is no subsequent rise in
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1990/12
Y1 - 1990/12
N2 - Interleukin-1 (IL-1) promotes cell recruitment and influences allergic mediator release. We analyzed histamine, prostaglandin D2, IL-1, and leukocytes accumulating hourly for 12 hours at skin-chamber sites after local ragweed challenge in eight allergic subjects with cutaneous late-phase reactions. Ragweed induced a peak of histamine at 1 hour (p<0.02), which diminished, and then steadily increased (p<0.02). Prostaglandin D2 levels peaked by the second hour (p<0.02) and then decreased, approaching prechallenge levels by 12 hours. Leukocyte infiltration (predominantly neutrophils) was detectable 3 to 4 hours after challenge, although selective enrichment of mononuclear cells, eosinophils, and basophils was observed at later hours (p<0.02). IL-1 bioactivity was detected in fluids 10 to 12 hours after challenge but not at control sites (p<0.05). Analysis of IL-1 β levels by RIA revealed an initial peak at 1 hour of 0.90 ng/ml (p<0.02) and a second elevation of up to 0.75 ng/ml during the later hours (p<0.04). Ragweed challenge of three nonatopic subjects did not change levels of the above-mentioned mediators or cells. Bioactivity in chamber fluids from antigen-challenged sites of atopic subjects was significantly neutralized by an anti-IL-1 β antiserum, although treatment with anti-IL-1 α and anti-IL-1 β was needed for complete neutralization. IL-1 released locally during cutaneous allergic reactions may contribute to IgE-dependent cutaneous inflammation.
AB - Interleukin-1 (IL-1) promotes cell recruitment and influences allergic mediator release. We analyzed histamine, prostaglandin D2, IL-1, and leukocytes accumulating hourly for 12 hours at skin-chamber sites after local ragweed challenge in eight allergic subjects with cutaneous late-phase reactions. Ragweed induced a peak of histamine at 1 hour (p<0.02), which diminished, and then steadily increased (p<0.02). Prostaglandin D2 levels peaked by the second hour (p<0.02) and then decreased, approaching prechallenge levels by 12 hours. Leukocyte infiltration (predominantly neutrophils) was detectable 3 to 4 hours after challenge, although selective enrichment of mononuclear cells, eosinophils, and basophils was observed at later hours (p<0.02). IL-1 bioactivity was detected in fluids 10 to 12 hours after challenge but not at control sites (p<0.05). Analysis of IL-1 β levels by RIA revealed an initial peak at 1 hour of 0.90 ng/ml (p<0.02) and a second elevation of up to 0.75 ng/ml during the later hours (p<0.04). Ragweed challenge of three nonatopic subjects did not change levels of the above-mentioned mediators or cells. Bioactivity in chamber fluids from antigen-challenged sites of atopic subjects was significantly neutralized by an anti-IL-1 β antiserum, although treatment with anti-IL-1 α and anti-IL-1 β was needed for complete neutralization. IL-1 released locally during cutaneous allergic reactions may contribute to IgE-dependent cutaneous inflammation.
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U2 - 10.1016/S0091-6749(05)80143-5
DO - 10.1016/S0091-6749(05)80143-5
M3 - Article
C2 - 2262641
AN - SCOPUS:0025696021
SN - 0091-6749
VL - 86
SP - 830
EP - 839
JO - The Journal of allergy and clinical immunology
JF - The Journal of allergy and clinical immunology
IS - 6 PART 1
ER -