Repeated application of glucocorticoids exacerbate pruritus via inhibition of prostaglandin D&lt;sub&gt;2&lt;/sub&gt; production of mast cells in a murine model of allergic contact dermatitis

Yamaura, Katsunori; Doi, Ryosuke; Suwa, Eriko; Ueno, Koichi

doi:10.2131/jts.37.1127

Cited by 12 publications

(9 citation statements)

References 33 publications

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“…Taken together, these observations suggest that the Tmem79 −/− phenotype does not include airway inflammation characteristic of the "atopic march" seen in some cases of AD (14). These results suggest that TMEM79 dysregulation promotes the accumulation of IL-17-expressing γδ-T cells and mast cells which have been implicated in AD (15,16) and pruritus (17)(18)(19).…”

Section: Resultsmentioning

confidence: 76%

Tissue-specific contributions of Tmem79 to atopic dermatitis and mast cell-mediated histaminergic itch

Emrick

Mathur

Wei

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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Atopic dermatitis (AD) is the most common skin disease in children. It is characterized by relapsing inflammation, skin-barrier defects, and intractable itch. However, the pathophysiology of itch in AD remains enigmatic. Here, we examine the contribution of Tmem79, an orphan transmembrane protein linked to AD in both mice and humans. We show that Tmem79 is expressed by both keratinocytes and sensory neurons, but that loss of keratinocytic Tmem79 is sufficient to elicit robust scratching. Tmem79−/− mice demonstrate an accumulation of dermal mast cells, which are diminished following chronic treatment with cyclooxygenase inhibitors and an EP3 receptor antagonist. In Tmem79−/− mice, mast cell degranulation produces histaminergic itch in a histamine receptor 1/histamine receptor 4 (H4R/H1R)-dependent manner that may involve activation of TRPV1− afferents. TMEM79 has limited sequence homology to a family of microsomal glutathione transferases and confers protection from cellular accumulation of damaging reactive species, and may thus play a role in regulating oxidative stress. In any case, mechanistic insights from this model suggest that therapeutics targeting PGE2 and/or H1R/H4R histaminergic signaling pathways may represent useful avenues to treat Tmem79-associated AD itch. Our findings suggest that individuals with mutations in Tmem79 develop AD due to the loss of protection from oxidative stress.

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Section: Resultsmentioning

confidence: 76%

Tissue-specific contributions of Tmem79 to atopic dermatitis and mast cell-mediated histaminergic itch

Emrick

Mathur

Wei

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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“…Cytokines representative of Th2 responses, including IL-4, IL-5, IL-10, and IL-13, are known to play important roles in CD. 17 Furthermore, it was reported that Th1-mediated cytokines, such as IL-12 and IFN-c, produced by Th1 cells acted as antagonists for these Th2 cytokines. 18,19 In the immediate allergic reaction phase, IgE produced, which is bound to the mast cell through the Fce receptor.…”

Section: Discussionmentioning

confidence: 99%

Coriander Alleviates 2,4-Dinitrochlorobenzene-Induced Contact Dermatitis-Like Skin Lesions in Mice

Park

Kim²,

Lim³

et al. 2014

Journal of Medicinal Food

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Contact dermatitis (CD) is a pattern of inflammatory responses in the skin that occurs through contact with external factors. The clinical picture is a polymorphic pattern of skin inflammation characterized by a wide range of clinical features, including itching, redness, scaling, and erythema. Coriandrum sativum L. (CS), commonly known as coriander, is a member of the Apiaceae family and is cultivated throughout the world for its nutritional and culinary values. Linoleic acid and linolenic acid in CS have various pharmacological activities. However, no study of the inhibitory effects of CS on CD has been reported. In this study, we demonstrated the protective effect of CS against 2,4-dinitrochlorobenzene-induced CD-like skin lesions. CS, at doses of 0.5-1%, applied to the dorsal skin inhibited the development of CD-like skin lesions. Moreover, the Th2-mediated inflammatory cytokines, immunoglobulin E, tumor necrosis factor-α, interferon-γ, interleukin (IL)-1, IL-4, and IL-13, were significantly reduced. In addition, CS increased the levels of total glutathione and heme oxygenase-1 protein. Thus, CS can inhibit the development of CD-like skin lesions in mice by regulating immune mediators and may be an effective alternative therapy for contact diseases.

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“…For TNCB administration, we used a modified version of the protocol by Yamaura et al [ 24 ], as illustrated in Figure 1 . Briefly, on Day 9, the abdomens of the mice were shaved, and two days later, 100 μL 1.0% TNCB solution in acetone ( w / v ) was applied to the shaved area for sensitization.…”

Section: Methodsmentioning

confidence: 99%

Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice

Cohen

Feldman-Goriachnik

Hanani

2022

Cells

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Itch (pruritus) is a common chronic condition with a lifetime prevalence of over 20%. The mechanisms underlying itch are poorly understood, and its therapy is difficult. There is recent evidence that following nerve injury or inflammation, intercellular communications in sensory ganglia are augmented, which may lead to abnormal neuronal activity, and hence to pain, but there is no information whether such changes take place in an itch model. We studied changes in neurons and satellite glial cells (SGCs) in trigeminal ganglia in an itch model in mice using repeated applications of 2,4,6-trinitro-1-chlorobenzene (TNCB) to the external ear over a period of 11 days. Treated mice showed augmented scratching behavior as compared with controls during the application period and for several days afterwards. Immunostaining for the activation marker glial fibrillary acidic protein in SGCs was greater by about 35% after TNCB application, and gap junction-mediated coupling between neurons increased from about 2% to 13%. The injection of gap junction blockers reduced scratching behavior, suggesting that gap junctions contribute to itch. Calcium imaging studies showed increased responses of SGCs to the pain (and presumed itch) mediator ATP. We conclude that changes in both neurons and SGCs in sensory ganglia may play a role in itch.

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Repeated application of glucocorticoids exacerbate pruritus via inhibition of prostaglandin D<sub>2</sub> production of mast cells in a murine model of allergic contact dermatitis

Cited by 12 publications

References 33 publications

Tissue-specific contributions of Tmem79 to atopic dermatitis and mast cell-mediated histaminergic itch

Tissue-specific contributions of Tmem79 to atopic dermatitis and mast cell-mediated histaminergic itch

Coriander Alleviates 2,4-Dinitrochlorobenzene-Induced Contact Dermatitis-Like Skin Lesions in Mice

Satellite Glial Cells and Neurons in Trigeminal Ganglia Are Altered in an Itch Model in Mice

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