| Journal | Date | IF | Authorship | doi |
|---|---|---|---|---|
| Cell host & microbe | Feb, 2024 | 30.3 | Co-Author | https://doi.org/10.1016/j.chom.2023.12.006 |
Skin microbe-dependent TSLP-ILC2 priming axis in early life is co-opted in allergic inflammation
Jimin Cha, Tae-Gyun Kim, Euihyun Bhae, Ho-Jin Gwak, Yeajin Ju, Young Ho Choe, In-Hwan Jang, Youngae Jung, Sungmin Moon, Taehyun Kim, Wuseong Lee, Jung Sun Park, Youn Wook Chung, Siyoung Yang, Yong-Kook Kang, Young-Min Hyun, Geum-Sook Hwang, Won-Jae Lee, Mina Rho, 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.