The University of Osaka · Medicine
Professor Yuumi Nakamura's research lab focuses on the intricate interplay between the skin immune system, the skin microbiota, and inflammatory skin diseases such as atopic dermatitis (AD) and cryopyrin-associated periodic syndrome (CAPS). The lab investigates how dysregulated innate immune responses—particularly involving interleukin-1β and interleukin-17—drive chronic inflammation, with a special emphasis on the roles of resident immune cells like mast cells and keratinocytes. Using clinical samples, animal models, and genomic analyses, the lab explores microbial colonization, quorum-sensing systems in *Staphylococcus aureus*, and host-microbe interactions that contribute to disease pathogenesis and immune regulation.
Figures are computed from collected data and may differ slightly.
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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