The University of Osaka · 의학
Yuumi Nakamura 교수의 연구실은 피부의 면역 반응과 미생물군 간 상호작용에 초점을 맞춘 피부면역학 전문 연구실입니다. 특히 아토피성 피부염 등 염증성 피부질환에서 병원성 박테리아(S. aureus), 곰팡이(Malassezia) 및 피부 미생물군의 역할과 그 기전을 면역세포(예: 마스트세포, 키라티노사이트)와 사이토카인(IL-1β, IL-17) 신호 경로를 중심으로 규명하고 있습니다. 또한, 피부의 면역 홈오스티시스 유지와 질병 발생 메커니즘을 이해하기 위해 임상적·모델 기반의 분자면역학적 접근을 융합적으로 수행하고 있습니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Urticarial rash observed in cryopyrin-associated periodic syndrome (CAPS) caused by nucleotide-binding oligomerization domain-leucine-rich repeats containing pyrin domain 3 (NLRP3) mutations is effectively suppressed by anti-interleukin (IL)-1 treatment, suggesting a pathophysiological role of IL-1beta in the skin. However, the cellular mechanisms regulating IL-1beta production in the skin of CAPS patients remain unclear. We identified mast cells (MCs) as the main cell population responsible for
Atopic dermatitis (AD) is commonly associated with colonization by <i>Staphylococcus aureus</i> in the affected skin. To understand the role of <i>S. aureus</i> in the development of AD, we performed whole-genome sequencing of <i>S. aureus</i> strains isolated from the cheek skin of 268 Japanese infants 1 and 6 months after birth. About 45% of infants were colonized with <i>S. aureus</i> at 1 month regardless of AD outcome. In contrast, skin colonization by <i>S. aureus</i> at 6 months of age in
Atopic dermatitis (AD) is a chronic inflammatory skin disease that affects 15-20% of children and 2-5% of adults in industrialized countries. The pathogen Staphylococcus aureus selectively colonizes the lesional skin of AD patients while this bacterium is absent in the skin of the majority of healthy individuals. However, the role of S. aureus in the pathogenesis of AD remains poorly understood. In addition to S. aureus, recent studies show a contribution of the skin microbiota to the regulation
The skin is home to various bacteria, archaea, fungi, and viruses, collectively referred to as the skin microbiota. Patients with certain skin diseases reportedly have unique skin "dysbiosis," a condition involving imbalanced microbiota, suggesting that dysbiosis in the skin may be either causal or a consequence of specific skin diseases. Atopic dermatitis (AD) is the most common allergic skin disease that affects 15-20% of children and 2-10% of adults worldwide. Both intrinsic genetic factors,
Using a new skin infection model, it is shown that Malassezia-induced IL-17- dependent skin inflammation and control of fungal infection are mediated via keratinocyte IL-36 receptor/MyD88 signaling.
IL-17 plays important roles in host defense against Candida albicans at barrier surfaces and during invasive infection. However, the role of IL-17 in host defense after colonization of the epidermis, a main site of C. albicans infection, remains poorly understood. Using a murine model of epicutaneous candidiasis without skin abrasion, we found that skin inflammation triggered by epidermal C. albicans colonization was self-limiting with fungal clearance completed by day 7 after inoculation in wil
Staphylococcus aureus can cause outbreaks and becomes multi-drug resistant through gene mutations and acquiring resistance genes. However, why S. aureus easily adapts to hospital environments, promoting resistance and recurrent infections, remains unknown. Here we show that a specific S. aureus lineage evolved from a clone that expresses the accessory gene regulator (Agr) system to subclones that reversibly suppressed Agr and caused an outbreak in the hospital setting. S. aureus with flexible Ag
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