<i>Ruminococcus gnavus</i> ameliorates atopic dermatitis by enhancing Treg cell and metabolites in BALB/c mice

  • Jae‐Rin Ahn
    Asan Institute for Life Sciences University of Ulsan College of Medicine Seoul Korea
  • Seung‐Hwa Lee
    Asan Institute for Life Sciences University of Ulsan College of Medicine Seoul Korea
  • Byunghyun Kim
    Korea Basic Science Institute Seoul Center Seoul Korea
  • Myung Hee Nam
    Korea Basic Science Institute Seoul Center Seoul Korea
  • Yoon Kyung Ahn
    Korea Basic Science Institute Western Seoul Center Seoul Korea
  • Yoon Mee Park
    Asan Institute for Life Sciences University of Ulsan College of Medicine Seoul Korea
  • Seon‐Mi Jeong
    Asan Institute for Life Sciences University of Ulsan College of Medicine Seoul Korea
  • Min Jee Park
    Department of Pediatrics Childhood Asthma Atopy Center Humidifier Disinfectant Health Center Asan Medical Center University of Ulsan College of Medicine Seoul Korea
  • Kun Baek Song
    Department of Pediatrics Childhood Asthma Atopy Center Humidifier Disinfectant Health Center Asan Medical Center University of Ulsan College of Medicine Seoul Korea
  • So‐Yeon Lee
    Department of Pediatrics Childhood Asthma Atopy Center Humidifier Disinfectant Health Center Asan Medical Center University of Ulsan College of Medicine Seoul Korea
  • Soo‐Jong Hong
    Department of Pediatrics Childhood Asthma Atopy Center Humidifier Disinfectant Health Center Asan Medical Center University of Ulsan College of Medicine Seoul Korea

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<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p><jats:italic>Ruminococcus gnavus</jats:italic> (<jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic>) are mucin‐degrading gut bacteria that play a key role in the early colonization of the gut by serving as endogenous sources of nutrients. They can also influence immune development. We had previously reported a lower abundance of <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> in infants with atopic dermatitis (AD) compared with that in healthy subjects. However, the underlying mechanisms remain unclear. In this study, we investigated the effect of orally administered <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> on antibiotic treatment‐induced gut dysbiosis (and the underlying mechanism) in a mouse model of AD.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Four‐week‐old female BALB/C mice were administered antibiotic cocktails for 2 weeks. <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> was orally administered throughout the study duration. At 6 weeks of age, AD was induced by epidermal sensitization with ovalbumin. AD phenotypes and systemic and gut immune responses were investigated.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Orally administered <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> significantly reduced AD‐associated parameters (i.e., transepidermal water loss, clinical score, total serum immunoglobulin (Ig) E level, OVA‐specific IgE level, and skin inflammation). <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> treatment also resulted in significant downregulation of T helper 2–related cytokine mRNA and upregulation of interleukin (IL)‐10 and Foxp3 in the skin. The population of CD4<jats:sup>+</jats:sup>FOXP3<jats:sup>+</jats:sup> T cells in mesenteric‐ and skin‐draining lymph nodes and butyrate levels in the cecum increased in <jats:italic>R</jats:italic>.<jats:italic> gnavus</jats:italic>‐administered AD mice.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Immune modulation by orally administered <jats:italic>R</jats:italic>. <jats:italic>gnavus</jats:italic> may alleviate AD symptoms through the enhancement of regulatory T‐cell counts and short‐chain fatty acids production in AD mice.</jats:p></jats:sec>

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