Enteric Nervous System-Derived VIP Restrains Differentiation of LGR5+ Stem Cells Towards the Secretory Lineage Impeding Type 2 Immune Programs
Intestinal epithelial homeostasis is sustained by the continuous differentiation of stem cells that are located at the bottom of theintestinal crypts. Epithelial renewal is a highly dynamic process that receives signaling input from various cellular systems to secure barrier function and nutrient uptake.
Here, we addressed the role of the enteric nervous system (ENS) in this process. We identify a pivotal function of the ENS in controlling epithelial proliferation, differentiation, and mucosal homeostasis. Neuronal Vasoactive Intestinal Peptide (VIP), acting via its receptor VIPR1 expressed by epithelial stem cells, restrains proliferation and differentiation towards the secretory lineage. Deficiency of VIP or VIPR1 led to an increase in secretory epithelial cells, including tuft cells, increased IL-25 expression, and activation of ILC2.
Functionally, VIP deficiency improved worm expulsion and exacerbated allergic lung inflammation. Our data expose a previously unappreciated role for the ENS in dictating epithelial cell fate decisions, thereby establishing a neuro-epithelial unit as a critical checkpoint for ILC2 and type 2 immunity, complementing the well-known regulators of barrier integrity and mucosal homeostasis, namely the commensal microbiota, the epithelial barrier, and the immune system.
Intestinal epithelial homeostasis is sustained by the continuous differentiation of stem cells that are located at the bottom of theintestinal crypts. Epithelial renewal is a highly dynamic process that receives signaling input from various cellular systems to secure barrier function and nutrient uptake.
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Here, we addressed the role of the enteric nervous system (ENS) in this process. We identify a pivotal function of the ENS in controlling epithelial proliferation, differentiation, and mucosal homeostasis. Neuronal Vasoactive Intestinal Peptide (VIP), acting via its receptor VIPR1 expressed by epithelial stem cells, restrains proliferation and differentiation towards the secretory lineage. Deficiency of VIP or VIPR1 led to an increase in secretory epithelial cells, including tuft cells, increased IL-25 expression, and activation of ILC2.
Functionally, VIP deficiency improved worm expulsion and exacerbated allergic lung inflammation. Our data expose a previously unappreciated role for the ENS in dictating epithelial cell fate decisions, thereby establishing a neuro-epithelial unit as a critical checkpoint for ILC2 and type 2 immunity, complementing the well-known regulators of barrier integrity and mucosal homeostasis, namely the commensal microbiota, the epithelial barrier, and the immune system.
Christoph Klose
Christoph Klose earned his Ph.D. in Molecular Medicine from Albert-Ludwigs-University in Freiburg in 2007. Following his doctoral studies, he conducted post-doctoral research at Weill Cornell Medicine in New York City before establishing an independent Emmy-Noether research group at the Department of Microbiology, Infectious Diseases, and Immunology of Charité — Universitätsmedizin Berlin.
Dr. Klose’s research has significantly contributed to our understanding of immune cell lineage commitment and development, with a particular focus on innate lymphoid cells (ILCs).
In recognition of his contributions, he was awarded the Robert Koch post-doctoral Immunology award in 2015 and has been listed as a Highly Cited Researcher by Clarivate Analytics since 2020. The main focus areas of his research group are (1) The interaction between the immune system and the nervous system, particularly at barrier surfaces, and (2) the role of ILC2s in type 2 immunity.
Christoph Klose earned his Ph.D. in Molecular Medicine from Albert-Ludwigs-University in Freiburg in 2007. Following his doctoral studies, he conducted post-doctoral research at Weill Cornell Medicine in New York City before establishing an independent Emmy-Noether research group at the Department of Microbiology, Infectious Diseases, and Immunology of Charité — Universitätsmedizin Berlin.
Dr. Klose’s research has significantly contributed to our understanding of immune cell lineage commitment and development, with a particular focus on innate lymphoid cells (ILCs).
Show more
In recognition of his contributions, he was awarded the Robert Koch post-doctoral Immunology award in 2015 and has been listed as a Highly Cited Researcher by Clarivate Analytics since 2020. The main focus areas of his research group are (1) The interaction between the immune system and the nervous system, particularly at barrier surfaces, and (2) the role of ILC2s in type 2 immunity.