Potential Role of Endothelin-1 in Atopic Dermatitis
AbstractPurpose of reviewAtopic dermatitis (AD) is a chronic eczematous skin disease associated with intense pruritus and skin barrier dysfunction. Not only histamine, but also various pruritogens can induce itch in the skin of AD patients. Among them, one of the potentially endogenous pruritogens in the skin is endothelin-1 (ET-1). To understand the mechanism of action, production, and roles of ET-1 in the skin of AD, we reviewed recent advances in the understanding of ET-1.Recent findingsRecently, functions of ET-1 related to inflammation other than itch have been reported. The expression of ET-1 and IL-25 was found to be coordinately upregulated in the lesional skin of AD patients and a murine AD model. IL-25 augmented ET-1 expression, and ET-1 reciprocally increased IL-25 expression in keratinocytes. In addition, ET-1 directly induced phenotypic and functional maturation of murine bone marrow –derived dendritic cells (DCs) and modified T cell responses.SummaryET-1 might be involved not only in pruritus but also in inflammation of AD. ET-1 may be a future target for antipruritic and anti-inflammatory agents in AD treatment.
Eczema, atopic dermatitis, urticaria, and other inflammatory allergic cutaneous reactions cause itch. Itch often makes the patients scratch their skin, and persistent scratching can aggravate dermal conditions. Itch can even cause emotional disturbance and sleep loss. The management of itch is therefore a key component of the clinical treatment of patients with allergies.
CONCLUSION: We present the case of allergic contact dermatitis (ACD) due to hypersensitivity to fentanyl with good tolerance to buprenorphine. Positive PT in this patient suggests a type IV hypersensitivity mechanism. Allergic reactions to opioids are frequently immediate, but delayed reactions could appear, especially when the drug is administered topically. PMID: 31131754 [PubMed - as supplied by publisher]
This paper explores the interrelationship of acute stress, itch, and scratching in patients with atopic dermatitis, providing new insights on the mechanism of stress-related exacerbation of itch.The British Journal of Dermatology
ConclusionsAdults with AD had low rates of outpatient and high rates of urgent care, ED, and hospital visits. The major predictor of outpatient utilization for AD care was AD severity. Racial/ethnic, socioeconomic, and/or health care disparities reduce outpatient utilization and increase urgent care, ED, and hospital utilization.
(NIH/National Institute of Allergy and Infectious Diseases) Scratching the skin triggers a series of immune responses culminating in an increased number of activated mast cells -- immune cells involved in allergic reactions -- in the small intestine, according to research conducted in mice. This newly identified skin-gut communication helps illuminate the relationship between food allergy and atopic dermatitis (a type of eczema), a disease characterized by dry, itchy skin. The NIAID-supported study was led by researchers at Boston Children's Hospital.
Neurogenic inflammation encompasses atopic dermatitis, allergy, inflammation and itch. Mas-related G-protein coupled receptors (Mrgprs) are increasingly recognized as critical to neurogenic inflammation. Substance P (SP) is an established mediator of neurogenic inflammation. Our hypothesis is that SP mediates its effects through MrgprA1. To test this hypothesis, we determined that neurons which respond to SP express MrgprA1. Furthermore, neurons from MrgprA1-/- mice generated using CRISPR/cas9 did not respond to SP.
In this study we used HPLC and LC/MS analysis, combined with a BATMAN-TCM platform, for detailed HPLC fingerprint analysis and network pharmacology of QP, and investigated the anti-inflammatory and antipruritic activities of QP on ACD induced by squaric acid dibutylester (SADBE) in mice. The BATMAN-TCM analysis provided information of effector molecules of the main ingredients of QP, and possible chronic dermatitis-associated molecules and cell signaling pathways by QP. In ACD mice, QP treatment suppressed the scratching behavior induced by SADBE in a dose-dependent manner and inhibited the production of Th1/2 cytokines in...
Atopic dermatitis (AD) is the most common chronic inflammatory skin disease, characterized by a fluctuating course, intense itch, and strongly inflamed skin lesions,1 putatively caused by a complex interaction of genetic, immune and environmental factors.2 AD is a highly heritable disease, showing strong associations with filaggrin (FLG) gene null mutations and Th2 signaling pathways,2 that have implications for epithelial barrier and skin inflammatory properties in affected individuals, respectively.
This article is protected by copyright. All rights reserved. PMID: 30895603 [PubMed - as supplied by publisher]
Atopic dermatitis (AD) is a chronic, predominantly type 2 inflammatory skin disease that affects up to 10% of adults and 20% of children [1 –5]. Moderate-to-severe AD is characterized by extensive eczematous lesions, pronounced persistent, severe itch [6–8], substantial pain and discomfort [9–12], and is frequently associated with other type 2 (atopic/allergic) comorbidities, e.g. asthma, allergic rhinitis, chronic rhinosinusitis with nasal polyposis (CRSwNP), eosinophilic esophagitis, and food allergies [8,13–15], and a significant disease burden, e.g.