TRPV4-Mediated Detection of Hyposmotic Stress by Skin Keratinocytes Activates Developmental Immunity
- Galindo-Villegas, J., Montalban-Arques, A., Liarte, S., de Oliveira, S., Pardo-Pastor, C., Rubio-Moscardo, F., Meseguer, J., Valverde, M.A., Mulero, V.
- Journal of immunology (Baltimore, Md. : 1950) 196(2): 738-49 (Journal)
- Registered Authors
- de Oliveira, Sofia, Galindo-Villegas, Jorge, Mulero, Victor
- MeSH Terms
- Embryo, Nonmammalian/immunology
- Fluorescent Antibody Technique
- Immunity, Innate/immunology*
- Osmotic Pressure
- Reverse Transcriptase Polymerase Chain Reaction
- TRPV Cation Channels/immunology*
- Zebrafish Proteins/immunology*
- 26673139 Full text @ J. Immunol.
Galindo-Villegas, J., Montalban-Arques, A., Liarte, S., de Oliveira, S., Pardo-Pastor, C., Rubio-Moscardo, F., Meseguer, J., Valverde, M.A., Mulero, V. (2016) TRPV4-Mediated Detection of Hyposmotic Stress by Skin Keratinocytes Activates Developmental Immunity. Journal of immunology (Baltimore, Md. : 1950). 196(2):738-49.
As an organism is exposed to pathogens during very early development, specific defense mechanisms must take effect. In this study, we used a germ-free zebrafish embryo model to show that osmotic stress regulates the activation of immunity and host protection in newly hatched embryos. Mechanistically, skin keratinocytes were responsible for both sensing the hyposmolarity of the aquatic environment and mediating immune effector mechanisms. This occurred through a transient potential receptor vanilloid 4/Ca(2+)/TGF-β-activated kinase 1/NF-κB signaling pathway. Surprisingly, the genes encoding antimicrobial effectors, which do not have the potential to cause tissue damage, are constitutively expressed during development, independently of both commensal microbes and osmotic stress. Our results reveal that osmotic stress is associated with the induction of developmental immunity in the absence of tissue damage and point out to the embryo skin as the first organ with full capacities to mount an innate immune response.
Errata / NotesThis article is corrected by ZDB-PUB-220906-41.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes