Skin eosinophilia in atopic patients

Hénocq, E; Vargaftig, B.B.

doi:10.1016/0091-6749(88)91040-8

Cited by 79 publications

(35 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The observation that atopic and non-atopic individuals respond similarly to intradermal PAF has been reported elsewhere (Henocq & Vargaftig, 1988). It was shown that the atopic and non-atopic subjects had a similar acute flare and weal response to PAF.…”

Section: Flare and Weal Reponsementioning

confidence: 58%

“…PAF also produces degranulation and aggregation of platelets (Henson, 1970;Kuster et al, 1986); whilst in intact tissue it causes vasoconstriction (Humphrey et al, 1982), extravasation (Humphrey et al, 1982;Hwang et al, 1985), bronchoconstriction (Cuss et al, 1986;Roberts et al, 1988) and cellular accumulation (Archer et al, 1985a;Henocq & Vargaftig, 1988). Its importance flare weal atopic as a putative primary mediator in asthma is the subject of much current research interest.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

Sciberras

Jordan

Gill

et al. 1991

Brit J Clinical Pharma

View full text Add to dashboard Cite

Section: Flare and Weal Reponsementioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

Sciberras

Jordan

Gill

et al. 1991

Brit J Clinical Pharma

View full text Add to dashboard Cite

“…Further, aerosolized LTB4 administered by inhalation to guinea-pigs was shown to induce eosinophil accumulation (Silbaugh et al, 1987) and a selective LTB4 antagonist to inhibit eosinophil accumulation induced by antigen challenge (Richards et al, 1989). PAF has been shown to be a potent mediator in stimulating human eosinophil chemotaxis in vitro and induces the accumulation of eosinophils when administered to a skin window chamber in man (Henocq & Vargaftig, 1988). Furthermore, the ability of PAF to mimic several aspects of antigen challenge including bronchoconstriction, increased bronchial reactivity and tissue oedema formation (reviewed in Braquet et al, 1987) (Silbaugh et al, 1987;Lellough-Tubiana et al, 1988;Richards et al, 1989;Gulbenkian et al, 1990).…”

Section: Resultsmentioning

confidence: 99%

“…Allergic patients have elevated levels of circulating eosinophils and these cells accumulate after antigenic challenge in the skin and airways (de Monchy et al, 1985;Henocq & Vargaftig, 1988;Lozewicz et al, 1991). There is now considerable evidence implicating the eosinophil in the pathophysiology of asthma.…”

Section: Introductionmentioning

confidence: 99%

Investigation of the endogenous chemoattractants involved in ¹¹¹In‐eosinophil accumulation in passive cutaneous anaphylactic reactions in the guinea‐pig

Weg

Watson

Faccioli

et al. 1994

British J Pharmacology

View full text Add to dashboard Cite

6LY1 Eosinophil accumulation and plasma extravasation are features of type I allergic responses. In an attempt to characterize the mediators of these responses, we have examined the local accumulation of "'In-eosinophils and leakage of '25I-human serum albumin ('251-HSA) during passive cutaneous anaphylaxis (PCA) reactions and in response to defined inflammatory mediators in the guinea-pig. Animals were passively sensitized by intradermal injection of anti-bovine gamma globulin antibody (50 fil, 1/50 dilution). After 20-24 h, animals were injected intravenously with '11In-eosinophils and '25I-HSA for the measurement of cell accumulation and plasma leakage, respectively. 2 When injected into sensitized sites, antigen caused a dose-related increase in the accumulation of "'In-eosinophils and plasma leakage in guinea-pig skin. Time course experiments over 24 h revealed that the maximal rate of "'In-eosinophil accumulation occurred over the first 90 min, with little accumulation at later time points. Plasma leakage was completed within the first 30 min after challenge. Responses to the mast cell degranulator, compound 48/80, exhibited very similar responses to the PCA reaction.3 Co-injection of antigen with the PAF antagonist, WEB 2086 (10-1 mol/site) or the 5-lipoxygenase inhibitor, PF 5901 (10-7mol/site) did not significantly alter the accumulation of "'In-eosinophils or plasma leakage, whereas these drug doses abolished responses to exogenous PAF (10-1 mol/site) and arachidonic acid (AA, 3 x I0-mol/site), respectively. The H, receptor antagonist chlorpheniramine (2.5 x 10-8 mol/site) did not reduce antigen-induced "'In-eosinophil accumulation. Drug combinations were also injected with antigen into sensitized sites, but were unable to reduce "'In-eosinophil accumulation. 4 These results indicate that anaphylactic eosinophil accumulation in this model involves mediators other than histamine, PAF or lipoxygenase products. This is in contrast to plasma leakage in this reaction, which can be abolished by a combination of antagonists blocking these mediators.

show abstract

“…Recent studies indicate a role for eosinophil disruption and degranulation in inducing tissue destruction and several potent, toxic protein in the granules, such as Major Basic Protein (MBP), Eosinophil-Derived Neurotoxin (EDN), Eosinophil Cationic Protein (ECP) and Eosinophil Peroxidase (EPO), are implicated in tissue damage associated with skin inflammation [9,10]. According with other Authors, we found elevated serum levels of ECP in children with AD, however no correlation between ECP serum levels and total IgE, as well as between ECP serum levels and the absolute number of peripheral blood eosinophils was shown [11].…”

Section: Allergic Inflammation In Atopic Dermatitis the Role Of Eosinmentioning

confidence: 99%

Atopic Dermatitis and Allergen Hypersensitivity: State of the Art

Cantani¹

2016

J Ped Moth Care

View full text Add to dashboard Cite

The current growing enthusiasm for atopic dermatitis is clearly reflected in the range of current attitudes on the subject. What are considered to be its protean manifestations are frequent challenges to the pediatrician and other specialists working with children. AD may occur not only in man, but also in other vertebrates. However, it must be assumed that AD has always been an affection of our species. Hippocrates (460-370 BC) reported urticaria and gastrointestinal upset following cow's milk ingestion. Lucretius (98-55 BC) wrote that one man's meat is another man's poison. Galen (131-219) described allergy to goat's milk. At the turn of this century the first description of acute shock due to CM allergy (CMA) and fatal CMA were published. In his pioneer studies of food allergy (FA), Schloss was the first to evaluate skin tests for the diagnosis of FA. Since then, a vast array of symptoms and disorders has been attributed to FA, many of which occur with other conditions. In addition to this, the lack of a single, practical diagnostic test has contributed to the polarization of the scientific controversy between those who believe in and those who deny FA existence. Terminology has also been confusing. A correct use of definitions is necessary for a proper epidemiologic evaluation of the conditions and an accurate diagnostic and therapeutic approach. While this concept was fundamentally correct, it was also too easily weakened by ignoring this prerequisite to be fully acceptable, and this led to an equally disordered use of the term hypersensitivity, since allergy had become a word used to embrace all possible forms of adverse reactions. AD is associated with patchy, characteristically distributed areas of cutaneous eczema, with intense itching and subsequent lichenification of the skin. Cutaneous automic dysfunction (increased vasoconstriction) and xerosis (dryness of the skin) commonly occur in the affected children. In addition, profound immunological dysregulation with various immune alterations has been described in affected children. Most children produce IgE antibodies to a number of food and inhalants allergens, at the point that a minuscule offending quantity can trigger a reaction by skin contact or by inhalation.

show abstract

Skin eosinophilia in atopic patients

Cited by 79 publications

References 17 publications

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

Investigation of the endogenous chemoattractants involved in ¹¹¹In‐eosinophil accumulation in passive cutaneous anaphylactic reactions in the guinea‐pig

Atopic Dermatitis and Allergen Hypersensitivity: State of the Art

Contact Info

Product

Resources

About

Skin eosinophilia in atopic patients

Cited by 79 publications

References 17 publications

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

The role of histamine in the acute inflammatory responses to intradermal platelet activating factor.

Investigation of the endogenous chemoattractants involved in 111In‐eosinophil accumulation in passive cutaneous anaphylactic reactions in the guinea‐pig

Atopic Dermatitis and Allergen Hypersensitivity: State of the Art

Contact Info

Product

Resources

About

Investigation of the endogenous chemoattractants involved in ¹¹¹In‐eosinophil accumulation in passive cutaneous anaphylactic reactions in the guinea‐pig