Chemical mediators in atopic dermatitis: Involvement of leukotriene B4 released by a type I allergic reaction in the pathogenesis of atopic dermatitis

Koro, Osamu; Furutani, Kiyoshi; Hide, Michihiro; Yamada, Satoru; Yamamoto, Shoso

doi:10.1016/s0091-6749(99)70240-x

Cited by 65 publications

(47 citation statements)

References 32 publications

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“…107 Several mediators of AD are released upon mast cell degranulation during the late phase of a type I allergic reaction, which then induce cellular infiltration, leading to more persistent symptoms. 108 Recent data reveal that both LTB 4 and CysLTs are crucial for the pathogenesis of AD, as follows: LTB 4 initiates the infiltration of neutrophils, eosinophils, and Th2 cells into the skin; CysLTs then induce the characteristic structural alterations associated with chronically affected skin, specifically skin fibrosis and keratinocyte proliferation. 109 Indeed, a number of studies report increased levels of LTB 4 in the skin lesions of patients with AD or allergic contact dermatitis.…”

Section: Ltb 4 and Atopic Dermatitismentioning

confidence: 99%

The role of leukotrienes in allergic diseases

Liu

Yokomizo

2015

Allergology International

137

106

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Leukotrienes (LTs), both LTB4 and the cysteinyl LTs (CysLTs) LTC4, LTD4 and LTE4, are implicated in a wide variety of inflammatory disorders. These lipid mediators are generated from arachidonic acid via multistep enzymatic reactions through which arachidonic acid is liberated from membrane phospholipids through the action of phospholipase A2. LTB4 and CysLTs exert their biological effects by binding to cognate receptors, which belong to the G protein-coupled receptor superfamily. LTB4 is widely considered to be a potent chemoattractant for most subsets of leukocytes, whereas CysLTs are potent bronchoconstrictors that have effects on airway remodeling. LTs play a central role in the pathogenesis of asthma and many other inflammatory diseases. This review will provide an update on the synthesis, biological function, and relevance of LTs to the pathobiology of allergic diseases, and examine the current and future therapeutic prospects of LT modifiers.

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Section: Ltb 4 and Atopic Dermatitismentioning

confidence: 99%

The role of leukotrienes in allergic diseases

Liu

Yokomizo

2015

Allergology International

137

106

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“…Neutrophils from AD patients have elevated LTA 4 H activity (Okano-Mitani et al, 1996), and release more LTB 4 in response to several stimuli (Hilger et al, 1991). LTB 4 concentrations are elevated in lesional skin of patients with AD (Fogh et al, 1989;Koro et al, 1999;Ruzicka et al, 1986;Thorsen et al, 1990). However, little is known about the role of LTB 4 in AD.…”

Section: Introductionmentioning

confidence: 99%

Leukotriene B4 Driven Neutrophil Recruitment to the Skin Is Essential for Allergic Skin Inflammation

Oyoshi

et al. 2013

Journal of Allergy and Clinical Immunology

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SummaryScratching triggers skin flares in atopic dermatitis (AD). We demonstrate that scratching of human skin, and tape stripping of mouse skin, causes neutrophil influx. This influx in mice was largely dependent on the generation of leukotriene B 4 (LTB 4 ) by neutrophils and their expression of the LTB 4 receptor BLT1. Allergic skin inflammation in response to epicutaneous (EC) application of ovalbumin to tape-stripped skin was severely impaired in Ltb4r1 −/− mice, and required expression of BLT1 on both T cells and non-T cells. Co-transfer of WT neutrophils, but not neutrophils deficient in BLT1 or the LTB 4 synthesizing enzyme LTA 4 H, restored the ability of WT CD4 + effector T cells to transfer allergic skin inflammation to Ltb4r1 −/− recipients. Pharmacologic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access

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“…Both cell pellets in test tube and residual cell in culture dishes were resolved in 1 ml of 0.25 N perchloric acid to recover all residual histamine. Histamine contents in the samples were measured fluorometrically by using an automated histamine analyzing system (Tosoh Corporation, Osaka, Japan) as described previously [11]. The histamine release was expressed as percentage of total cellular histamine.…”

Section: Measurement Of Histaminementioning

confidence: 99%