한빛사논문
Jimin Cha,1,13 Tae-Gyun Kim,2,3,13 Euihyun Bhae,4 Ho-Jin Gwak,5 Yeajin Ju,6 Young Ho Choe,7 In-Hwan Jang,8 Youngae Jung,6 Sungmin Moon,1 Taehyun Kim,1 Wuseong Lee,1 Jung Sun Park,9 Youn Wook Chung,1 Siyoung Yang,10 Yong-Kook Kang,9 Young-Min Hyun,7 Geum-Sook Hwang,6,12 Won-Jae Lee,8 Mina Rho,5,11 and Ji-Hwan Ryu 1,14,*
1Department of Biomedical Sciences, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul 03722, Korea
2Department of Dermatology, Severance Hospital, Cutaneous Biology Research Institute, Yonsei University College of Medicine, Seoul 03722, Korea
3Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul 03722, Korea
4Department of Artificial Intelligence, Hanyang University, Seoul 04763, Korea
5Department of Computer Science, Hanyang University, Seoul 04763, Korea
6Integrated Metabolomics Research Group, Western Seoul Center, Korea Basic Science Institute, Seoul 03759, Korea
7Department of Anatomy and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Korea
8National Creative Research Initiative Center for Hologenomics and School of Biological Sciences, Seoul National University, Seoul 08826, Korea
9Development and Differentiation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yuseong-gu, Daejeon 34141, Korea
10Department of Biological Sciences, Sungkyunkwan University, Suwon 16419, Korea
11Department of Biomedical Informatics, Hanyang University, Seoul 04763, Korea
12College of Pharmacy, Chung-Ang University, Seoul 06974, Korea
13These authors contributed equally
14Lead contact
*Corresponding author: correspondence to Ji-Hwan Ryu
Abstract
Although early life colonization of commensal microbes contributes to long-lasting immune imprinting in host tissues, little is known regarding the pathophysiological consequences of postnatal microbial tuning of cutaneous immunity. Here, we show that postnatal exposure to specific skin commensal Staphylococcus lentus (S. lentus) promotes the extent of atopic dermatitis (AD)-like inflammation in adults through priming of group 2 innate lymphoid cells (ILC2s). Early postnatal skin is dynamically populated by discrete subset of primed ILC2s driven by microbiota-dependent induction of thymic stromal lymphopoietin (TSLP) in keratinocytes. Specifically, the indole-3-aldehyde-producing tryptophan metabolic pathway, shared across Staphylococcus species, is involved in TSLP-mediated ILC2 priming. Furthermore, we demonstrate a critical contribution of the early postnatal S. lentus-TSLP-ILC2 priming axis in facilitating AD-like inflammation that is not replicated by later microbial exposure. Thus, our findings highlight the fundamental role of time-dependent neonatal microbial-skin crosstalk in shaping the threshold of innate type 2 immunity co-opted in adulthood.
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