They also downregulate antimicrobial peptides. Studies have shown that interleukin-4 and 13 are the leading type 2 cytokines that are able to downregulate filaggrin and other barrier molecules.
These are going to be your interleukin-4, interleukin-13, and interleukin-31, which is the itch cytokine, as well as well as the type 22 pathway. We have activation of immune molecules, particularly type 2 cytokine activation. We also have the immune component that we know now plays a huge role in atopic dermatitis.
#Peter lio skin#
We also see in the skin barrier in the stratum corneum abnormalities in the junctions in the skin. That’s a structural protein that is responsible for the stratum corneum homeostasis, and when we have these abnormalities or mutations in filaggrin, we see increases in transepidermal water loss and reductions in skin hydration. We also have the filaggrin mutations that I mentioned earlier. This is due to changes in ceramide composition, so lipids, and decreases in levels of total ceramides. Going a little bit more in depth with each of those, as I mentioned with the first model, the outside-in, the epidermal, we do have barrier defects in atopic dermatitic skin. We know now that these 2 different models are not mutually exclusive, and we have components of both. The other model is the immune-based model, or the inside-out model, and this model suggests that abnormal epidermal phenotype in lesional atopic dermatitis skin was infiltrated or initiated by the increased expression of cytokines that induce the epidermal abnormalities. This hypothesis really received a revival in 2006 when the filaggrin mutation was found. Then the immune activation was considered secondary in this model. The first was the epidermal-based model or the outside-in model, and this suggested that atopic dermatitis was all about genetic epidermal barrier defects that triggered abnormal keratinocyte hyperplasia. Historically, there were 2 competing pathophysiologic principles. McConaha, PharmD, NCTTP, BCACP, CDE: The pathophysiology of atopic dermatitis is somewhat complex. What is the pathophysiology of atopic dermatitis, and what is the typical age of onset? Can we start with Jamie? We’re going to begin with an overview of atopic dermatitis. Today we are going to talk about several topics pertaining to atopic dermatitis, including an overview of atopic dermatitis, unmet needs regarding treatment, the potential use of JAK inhibitors in atopic dermatitis management, and the critical role of pharmacists. Joining me today in this virtual discussion are: Dr Kristen Demundo, supervising pharmacist at Long Island Apothecary in Commack, New York Dr Jamie McConaha, associate professor of pharmacy practice at Duquesne University School of Pharmacy in Pittsburgh, Pennsylvania and Dr Shannon Rotolo, clinical pharmacy specialist at University of Chicago Medicine in Chicago, Illinois. I’m a clinical assistant professor of dermatology and pediatrics at Northwestern University Feinberg School of Medicine in Chicago, Illinois. Peter Lio, MD: Hello and welcome to this Pharmacy Times® Peer Exchange, “Potential Role of JAK Inhibitors in Atopic Dermatitis Treatment.” My name is Dr Peter Lio.
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