Sequential patterns of inflammatory events during developing and expressed skin late-phase reactions

Background: Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR. Objective: Our purpose was to compare sequential gros...

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Published inJournal of allergy and clinical immunology Vol. 105; no. 4; pp. 776 - 781
Main Authors Zweiman, Burton, Haralabatos, Irene C., Pham, Ngoc-Chân, David, Mary, von Allmen, Carolyn
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.04.2000
Elsevier
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ISSN0091-6749
DOI10.1067/mai.2000.105223

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Abstract Background: Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR. Objective: Our purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge. Methods: Gross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours. Results: Gross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P = .04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P < .01). Eosinophil accumulation was significant, starting at 1 hour (P < .001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG2+). T-cell accumulation started at 2 hours (P = .01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P < .005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent. Conclusions: Skin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR. (J Allergy Clin Immunol 2000;105:776-81.)
AbstractList Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR.BACKGROUNDAlthough there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR.Our purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge.OBJECTIVEOur purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge.Gross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours.METHODSGross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours.Gross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P =.04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P <.01). Eosinophil accumulation was significant, starting at 1 hour (P <.001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG(2)(+)). T-cell accumulation started at 2 hours (P =.01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P <.005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent.RESULTSGross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P =.04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P <.01). Eosinophil accumulation was significant, starting at 1 hour (P <.001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG(2)(+)). T-cell accumulation started at 2 hours (P =.01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P <.005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent.Skin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR.CONCLUSIONSSkin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR.
Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR. Our purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge. Gross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours. Gross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P =.04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P <.01). Eosinophil accumulation was significant, starting at 1 hour (P <.001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG(2)(+)). T-cell accumulation started at 2 hours (P =.01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P <.005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent. Skin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR.
Background: Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR. Objective: Our purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge. Methods: Gross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours. Results: Gross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P = .04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P < .01). Eosinophil accumulation was significant, starting at 1 hour (P < .001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG2+). T-cell accumulation started at 2 hours (P = .01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P < .005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent. Conclusions: Skin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR. (J Allergy Clin Immunol 2000;105:776-81.)
Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens, much less is known about the events occurring during development of such LPR. Our purpose was to compare sequential gross and histologic inflammatory responses during developing skin LPR within 6 hours after challenge. Gross reactions were measured and biopsy specimens obtained at 20 minutes and 1, 2, and 6 hours after intradermal allergen (Ag) and buffer diluent control (B) injections in 7 atopic subjects with known immediate and LPR. Inflammatory cell responses were compared, as detected by immunohistochemistry in Ag and B sites. These findings were then compared with those at 24 hours. Gross LPR evolved without a hiatus from the immediate wheal responses over the next 6 hours (P = .04 vs that in B sites) and then decreased by 24 hours. Prominent PMN accumulation started by 20 minutes, peaking at 1 hour (P < .01). Eosinophil accumulation was significant, starting at 1 hour (P < .001) and peaking at 6 hours (P < .001). Many eosinophils were activated (EG sub(2) super(+)). T-cell accumulation started at 2 hours (P = .01) and was most prominent at 24 hours. The frequency of vessels expressing E-selectin increased at 1 hour (P < .005), correlating with the degree of local PMN accumulation. The frequency of vessels expressing vascular cell adhesion molecules started increasing at 6 hours (P = .02), well after eosinophil accumulation was prominent. Skin LPR is characterized by evolution of a gross indurated reaction from the immediate whealing response over the first 6 hours after intradermal Ag challenge, with an early accumulation of PMN and eosinophils, not directly attributable to lymphocyte entry or vascular cell adhesion molecule expression. Likely, multiple other factors may also play roles in the complex pathogenesis of LPR.
Author Pham, Ngoc-Chân
von Allmen, Carolyn
Haralabatos, Irene C.
Zweiman, Burton
David, Mary
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Issue 4
Keywords B
lymphocytes
Late-phase reaction
Ag
Eos
eosinophils
mRNA
mast cells
LPR
VCAM
adhesion molecules
CLA
neutrophils
Human
Immunopathology
Allergy
Late
Immune response
Pathophysiology
Hypersensitivity
Granulocyte
Inflammation
Intradermal administration
Reaction
Eosinophil
Mast cell
Skin
Neutrophil
Lymphocyte
Allergen
Skin test
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Snippet Background: Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of...
Although there has been much study of the histologic features of the late-phase reactions (LPR) seen 6 to 24 hours after intradermal injection of allergens,...
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StartPage 776
SubjectTerms adhesion molecules
Adult
Allergological tests
Biological and medical sciences
Biopsy
Blood Proteins - analysis
Cell Adhesion Molecules - biosynthesis
Dermatitis - immunology
E-Selectin - analysis
Eosinophil Granule Proteins
eosinophils
Eosinophils - chemistry
Eosinophils - cytology
Humans
Hypersensitivity, Delayed - immunology
Hypersensitivity, Immediate - immunology
Immunological methods for diagnosis and exploration
Immunopathology
Intradermal Tests
Late-phase reaction
lymphocytes
mast cells
Medical sciences
Muscle, Smooth, Vascular - chemistry
Muscle, Smooth, Vascular - cytology
neutrophils
Neutrophils - cytology
Ribonucleases
Skin - immunology
Skin - pathology
Skin Tests
T-Lymphocytes - cytology
Title Sequential patterns of inflammatory events during developing and expressed skin late-phase reactions
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0091674900978047
https://dx.doi.org/10.1067/mai.2000.105223
https://www.ncbi.nlm.nih.gov/pubmed/10756229
https://www.proquest.com/docview/17532843
https://www.proquest.com/docview/71034943
Volume 105
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