Evaluation of the atopy patch test and the cutaneous late-phase reaction as relevant models for the study of allergic inflammation in patients with atopic eczema☆☆☆★

Langeveld-Wildschut, Elisabeth G.; Thepen, Theo; Biharia, Ilse C.; Reijsen, Frank C. van; Bruijnzeel, P. L. B.; Bruijnzeel-Koomen, Carla A.F.M.

doi:10.1016/s0091-6749(96)80186-2

Cited by 66 publications

(45 citation statements)

References 24 publications

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“…13,14,34 We have confirmed that the antiIgE-induced LPR in healthy research dogs are grossly and microscopically similar to allergen-induced LPR in dogs with AD 13 as well as to allergen and anti-IgE-induced LPR in humans. 16,[35][36][37] We have shown that anti-IgEinduced canine LPR exhibit increases in the mRNA transcription of several mediators typical of Th2-dominated responses, notably IL-13, IL-5, CCL5 and CCL17. It was also demonstrated that these cellular and mediator responses can be inhibited by prednisolone therapy, in a manner similar to that seen in allergen-induced LPR in humans.…”

Section: Discussionmentioning

confidence: 97%

“…Similar changes have been reported in biopsies taken after intradermal injection of allergen in humans. 35,42,43 Injection of anti-IgE resulted in a rapid influx of inflammatory cells. The observed biphasic increase in granulocytes followed by mononuclear cells (including both CD1c + dendritic cells and CD3 + lymphocytes) is typical of those described in LPR after injection of allergen or anti-IgE in both dogs 13 and humans.…”

Section: Discussionmentioning

confidence: 99%

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A canine model of cutaneous late‐phase reactions: prednisolone inhibition of cellular and cytokine responses

Pucheu‐Haston

Shuster²,

Olivry

et al. 2005

Immunology

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SummaryImmunoglobulin E (IgE)-mediated late-phase reactions can be induced in atopic humans by intradermal injection of relevant allergens or anti-IgE antibodies. The histology of these reactions resembles that of naturally occurring atopic dermatitis. Strikingly similar responses can be induced in dogs, suggesting that a canine model could prove valuable for preclinical investigation of drugs targeting late-phase reactions. This study was designed to characterize the cellular, cytokine and chemokine responses after intradermal anti-IgE injection in untreated and prednisolone-treated dogs. Normal beagles were untreated or treated with prednisolone before intradermal injection of polyclonal rabbit anti-canine IgE or normal rabbit IgG. Biopsies were taken before injection and 6, 24 and 48 hr after injection. Samples were evaluated by histological and immunohistochemical staining, as well as by real-time quantitative polymerase chain reaction analysis. Dermal eosinophil and neutrophil numbers increased dramatically within 6 hr after injection of rabbit anti-canine IgE, and remained moderately elevated at 48 hr. The numbers of CD1c + and CD3 + mononuclear cells were also increased at 6 hr. The real-time quantitative polymerase chain reaction demonstrated marked increases in mRNA expression for interleukin-13 (IL-13), CCL2, CCL5 and CCL17. Levels of mRNA for IL-2, IL-4, IL-6 and IFN-c did not change within the limits of detection. Prednisolone administration suppressed the influx of neutrophils, eosinophils, CD1c + and CD3 + cells, as well as expression of IL-13, CCL2, CCL5 and CCL17. These data document the cytokine and chemokine responses to anti-IgE injection in canine skin, and they demonstrate the ability of the model to characterize the anti-inflammatory effects of a known therapeutic agent.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

A canine model of cutaneous late‐phase reactions: prednisolone inhibition of cellular and cytokine responses

Pucheu‐Haston

Shuster²,

Olivry

et al. 2005

Immunology

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“…Langerhans cells express all three known types of IgE receptors: the low-affinity receptor (FcεRII or CD23), the high-affinity receptor (FcεRI), and the epsilon-binding protein (εBP) [60]. In already sensitized individuals, an association between allergen-specific serum IgE and positive APT reactions has been reported [21, 61, 62, 63]. It has been suggested that a positive APT reaction requires the presence of epidermal IgE+ Langerhans cells in clinically noninvolved skin, but that other yet unknown factors are also involved [63].…”

Section: Possible Pathogenic Mechanismsmentioning

confidence: 99%

Atopic Eczema/Dermatitis Syndrome and <i>Malassezia</i>

Scheynius

Johansson

Buentke

et al. 2002

Int Arch Allergy Immunol

118

133

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Atopic dermatitis is a chronic multifactorial inflammatory skin disease, which has had a marked increase in prevalence during the last decades. Recently, a new nomenclature was recommended where the term ‘atopic eczema/dermatitis syndrome’ (AEDS) should be used to reflect the heterogeneity in this group of patients and where those patients without measurable IgE reactivity should be classified as either ‘nonallergic AEDS’ or ‘non-IgE-associated allergic AEDS’. For nearly 20 years it has been discussed whether the opportunistic yeast Malassezia, previously designated Pityrosporum, is a contributing factor to AEDS. Today there are several reports that demonstrate specific serum IgE or positive skin prick test and/or atopy patch test reactions to Malassezia in patients with AEDS. Several IgE-binding components have been identified in extracts of Malassezia ranging in molecular mass between 10 and 100 kD. The genes for nine Malassezia allergens with molecular weights ranging from 14 to 36 kD have hitherto been identified and cloned. Six of them are now produced by recombinant techniques and used in diagnostic tests. At present the genus Malassezia is subdivided into seven different species, which all have been isolated from human skin. The respective contribution of different Malassezia spp. to AEDS and in what proportion they share allergens remains to be clarified. We summarize here data that Malassezia can play a role in eliciting and maintaining eczema in patients with AEDS.

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“…We therefore used the patch test as the method of antigen challenge. In the time course reaction after the patch test of aeroallergens in AE patients, eosinophil infiltration has been demonstrated to start as early as 2–6 h post-antigen challenge and to peak at 24–48 h [24,25,26]. We considered that a time point of 24 h after patch test might reflect the peak in the kinetics of eosinophil accumulation in the lesional skin.…”

Section: Introductionmentioning

confidence: 99%

Increased Expression of RANTES, CCR3 and CCR5 in the Lesional Skin of Patients with Atopic Eczema

Kato

Pawankar

Kimura

et al. 2006

Int Arch Allergy Immunol

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Background: Atopic eczema (AE) is a relapsing inflammatory disease based on IgE sensitization and characterized by peripheral blood eosinophilia and eosinophil infiltration into the lesional skin. In the patch test reaction of AE by allergens, an increased infiltration of activated eosinophils has been demonstrated peaking at 24–48 h. Regulated on activation normal T cell expressed and secreted (RANTES/CCL5) is a chemokine that induces eosinophil migration, and CCR3 and CCR5 are the receptors of RANTES. Objective: In order to further clarify the pathomechanisms of eosinophil infiltration in ongoing chronic inflammation in the skin of patients with AE and its relation to disease severity, we examined the expression of RANTES and its receptors CCR3 and CCR5 in challenged and unchallenged lesional skin of AE. Methods: We examined the number of RANTES+ cells, CCR3+ cells, CCR5+cells, activated (EG2+) eosinophils and CD3+ T cells in normal skin of healthy volunteers, and in challenged lesional skin (24 h after mite patch test) as well as unchallenged lesional skin of AE patients by immunohistochemistry. The cellular source of RANTES, CCR3 and CCR5 was analyzed by double immunohistochemistry using specific antibodies to RANTES, CCR3 or CCR5, and antibodies to ECP (EG2) or CD3. Results: The numbers of RANTES+ cells, CCR3+ cells, CCR5+ cells, EG2+ cells and CD3+ cells were all significantly increased in challenged (mite patch-tested) lesional skin of AE patients as compared to those in unchallenged lesional skin and normal skin. The numbers of these cells in unchallenged lesional skin were greater than those in normal skin. The number of EG2+ cells in the unchallenged lesional skin correlated with both the peripheral blood eosinophil count and the SCORAD index. The number of EG2+ cells in challenged lesional skin correlated with the number of CCR5+ cells. Activated eosinophils and T cells expressed RANTES and various proportions of these cells were CCR3+ and CCR5+ in both challenged and unchallenged lesional skin. Conclusion: Taken together, these results suggest that RANTES as well as its receptors CCR3 and CCR5 may play important roles in the orchestration of eosinophil infiltration in ongoing chronic inflammation in AE, and also reflect the severity of disease.

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Evaluation of the atopy patch test and the cutaneous late-phase reaction as relevant models for the study of allergic inflammation in patients with atopic eczema☆☆☆★

Cited by 66 publications

References 24 publications

A canine model of cutaneous late‐phase reactions: prednisolone inhibition of cellular and cytokine responses

A canine model of cutaneous late‐phase reactions: prednisolone inhibition of cellular and cytokine responses

Atopic Eczema/Dermatitis Syndrome and <i>Malassezia</i>

Increased Expression of RANTES, CCR3 and CCR5 in the Lesional Skin of Patients with Atopic Eczema

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