Publications by authors named "Chanisa Kiatsurayanon"

Background: Hori's nevus is a common and challenging dermatological condition, often complicated by post-inflammatory hyperpigmentation following treatment. Platelet-rich plasma (PRP) has demonstrated efficacy in the treatment of hyperpigmentation disorders such as melasma and periorbital darkening. Given the benefits and minimally invasive nature of PRP treatments, exploring its application in managing Hori's nevus through further investigation is worthwhile.

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Antimicrobial peptides (AMPs), also known as host defense peptides, are ubiquitous naturally occurring molecules secreted by various cell types of the body. In the skin, AMPs serve as a first-line innate immune defense against exogenous microorganisms, and they orchestrate adaptive immune responses to exert several immunomodulatory functions. Emerging evidence indicates that AMPs not only contribute to certain inflammatory skin diseases but also play a role in skin tumor carcinogenesis.

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Host defense peptides (HDPs) or antimicrobial peptides (AMPs) are short cationic amphipathic peptides of divergent sequences, which are part of the innate immune system and produced by various types of cells and tissues. The predominant role of HDPs is to respond to and protect humans against infection and inflammation. Common human HDPs include defensins, cathelicidin, psoriasin, dermcidin, and ribonucleases, but these peptides may be dysregulated in the skin of patients with atopic dermatitis (AD).

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Itch or pruritus is the hallmark of atopic dermatitis and is defined as an unpleasant sensation that evokes the desire to scratch. It is also believed that itch is a signal of danger from various environmental factors or physiological abnormalities. Because histamine is a well-known substance inducing itch, H-antihistamines are the most frequently used drugs to treat pruritus.

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Atopic dermatitis (AD) is a chronic relapsing inflammatory cutaneous disease that is often associated with other atopic symptoms, such as food allergy, allergic rhinitis and asthma, leading to significant morbidity and healthcare costs. The pathogenesis of AD is complicated and multifactorial. Although the aetiology of AD remains incompletely understood, recent studies have provided further insight into AD pathophysiology, demonstrating that the interaction among genetic predisposition, immune dysfunction and environmental provocation factors contributes to its development.

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Atopic dermatitis (AD) is a common chronic inflammatory skin disease that exhibits a complex interplay of skin barrier disruption and immune dysregulation. Patients with AD are susceptible to cutaneous infections that may progress to complications, including staphylococcal septicemia. Although most studies have focused on filaggrin mutations, the physical barrier and antimicrobial barrier also play critical roles in the pathogenesis of AD.

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Article Synopsis
  • Atopic dermatitis (AD) is a common chronic skin disease influenced by genetics, skin barrier issues, immune responses, allergies, and infections.
  • Bacterial and viral infections worsen AD symptoms, but research on fungal infections like Malassezia and Candida is limited despite their potential impact.
  • The review discusses the epidemiology, causes, symptoms, and often-missed aspects of fungal infections in AD, including diagnosis and treatment effectiveness.
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is a common non- species found in patients with candidiasis and it sometimes develops antifungal resistance. Human beta-defensin-3 (hBD-3) is an antimicrobial peptide of immune system active against various types of microbes including . This study investigated antifungal activity of hBD-3 and its synergistic effect with a first-line antifungal agent on clinical isolates.

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The epidermis functions as a first-line defense barrier that protects the body from the external environment. As a chemical hindrance, the epidermis possesses acidic pH, highly organized lipids and various host defense peptides, also known as antimicrobial peptides. Human β-defensins (hBDs), one of the most important host defense peptide families found in our skin, are well-known for their broad-spectrum microbicidal activities.

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Background: In addition to their microbicidal properties, host defense peptides (HDPs) display various immunomodulatory functions, including keratinocyte production of cytokines/chemokines, proliferation, migration and wound healing. Recently, a novel HDP named AMP-IBP5 (antimicrobial peptide derived from insulin-like growth factor-binding protein 5) was shown to exhibit antimicrobial activity against numerous pathogens, even at concentrations comparable to those of human β-defensins and LL-37. However, the immunomodulatory role of AMP-IBP5 in cutaneous tissue remains unknown.

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Punctate palmoplantar keratoderma (PPPK) is a rare entity with an estimated prevalence rate of 1.17/100,000. PPPK usually presents with bilateral asymptomatic, tiny, hyperkeratotic punctate papules and plaques on the palmoplantar surface.

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Host defense peptides/proteins (HDPs), also known as antimicrobial peptides/proteins (AMPs), are key molecules in the cutaneous innate immune system. AMPs/HDPs historically exhibit broad-spectrum killing activity against bacteria, enveloped viruses, fungi and several parasites. Recently, AMPs/HDPs were shown to have important biological functions, including inducing cell proliferation, migration and differentiation; regulating inflammatory responses; controlling the production of various cytokines/chemokines; promoting wound healing; and improving skin barrier function.

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Background: In addition to their antimicrobial activities, antimicrobial peptides, also known as host defense peptides (HDPs) activate keratinocytes; promote wound healing; and improve the skin barrier. AG-30/5C is a novel angiogenic HDP that activates various functions of fibroblasts and endothelial cells, including cytokine/chemokine production and wound healing.

Objectives: To investigate whether AG-30/5C activates human keratinocytes and to examine the underlying mechanisms.

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Background: Interleukin (IL)-37, a new member of the IL-1 family, is characterized as a fundamental inhibitor of innate immunity: it dampens the production of proinflammatory cytokines, protects against inflammatory and autoimmune diseases, and plays a potent immunosuppressive role in the pathogenesis of psoriasis. IL-37 is highly expressed in psoriatic skin, in which human β-defensins (hBDs) have been detected. Although hBDs enhance the production of cytokines, including IL-1 cytokines, whether they stimulate the production of IL-37 remains unclear.

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Both psoriasis and atopic dermatitis (AD) are not only associated with an impaired stratum corneum barrier, but also with abnormal expression of the tight junction (TJ) proteins. Because host defense peptides, including LL-37, are overexpressed in lesional psoriatic skin but are downregulated in lesional AD skin, we hypothesized that LL-37 might regulate the TJ function in keratinocytes. We demonstrated that LL-37 selectively increased the expression of several claudins and occludin, and enhanced their membrane distribution.

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Human β-defensins (hBDs) are host defense peptides that not only exhibit microbicidal properties but also stimulate various cellular activities, including keratinocyte proliferation, migration, and wound healing. hBDs are overexpressed in the skin in cases of psoriasis but are downregulated in atopic dermatitis skin, although both diseases are associated with stratum corneum barrier defects. Because the tight-junction (TJ) barrier is also dysfunctional in both atopic dermatitis and psoriasis patients, we hypothesized that hBDs may regulate the TJ barrier function in keratinocytes.

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