Communications Biology· 2026Q1
Chil4 regulates basal cell activation and neuronal differentiation in olfactory epithelium regeneration
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- Q1SCImago
- 2026year
Short summary
Chil4 deficiency in mice leads to zone-specific defects in olfactory neuron regeneration, increased basal cell populations, delayed horizontal basal cell activation, and enhanced inflammatory cell recruitment.
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Key points
- Chil4 deficiency causes zone-specific attenuation of neuronal regeneration in the olfactory epithelium.
- Chil4-deficient mice show increased globose basal cells and delayed horizontal basal cell activation after injury.
- Inflammatory cell recruitment (CD45+) is enhanced in the regenerating olfactory epithelium of Chil4-deficient mice.
- scRNA-seq data suggest DNA replication and cell cycle genes are upregulated in activated horizontal basal cells in Chil4-deficient mice, mediated by the Cd6-Alcam pair and CD4+ T cells.
- Notch-Hes1 signaling drives biased sustentacular cell regeneration in Chil4-deficient mice, which can be counteracted by γ-secretase inhibitors.
AI-generated from the title and abstract; the full text is not read.
Abstract
The mammalian olfactory epithelium (OE) exhibits remarkable capacity for continuous regeneration. Our previous work demonstrated that Chitinase-like 4 (Chil4) regulated regeneration in the injured OE. Expanding upon these findings, here we reported that Chil4 deficiency resulted in zone-specific attenuation of neuronal regeneration, increased population of globose basal cells (GBCs), delayed horizontal basal cell (HBC) activation post injury, and enhanced recruitment of CD45+ inflammatory cells to the regenerating OE. Moreover, scRNA-seq data support that DNA replication and cell cycle-related genes were upregulated in Krt6a+ activated HBCs, and Cd6-Alcam pair contributed to cell cycle progression of activated HBCs in the Chil4−/− OE by Cd4+ T cells. The biased sustentacular cell regeneration induced by Chil4 deletion was mediated by Notch-Hes1 signaling, and γ-secretase inhibitor LY411575 enhanced neuronal differentiation and inhibited sustentacular cell regeneration in the Chil4−/− OE. Collectively, this study elucidates critical events underlying the Chil4 deficiency in OE regeneration. These findings provide insights into the complex molecular mechanisms governing olfactory epithelium regeneration. Chil4 regulates horizontal basal cell activation, sensory neuronal and sustentacular cell differentiation, and inflammatory cell recruitment in the olfactory epithelium post injury, revealing a complex mechanism underlying olfactory epithelium regeneration.
The authors' abstract, as published at the source. Communications Biology, 2026 · DOI ↗
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