Plos iconPlosSep 22, 2026 ~1 min source read

Pathogen subversion of neuro-epidermal signaling impairs lysosomal function to disrupt collagen homeostasis in <i>Caenorhabditis elegans</i>

by Qian Li, Yating Liu, Hanyi Chen, Weilie Xiao, Bin Qi The epidermis relies on collagen-rich extracellular matrices (ECMs) to maintain barrier integrity against pathogens. Using Pseudomonas aeruginosa PA14- Caenorhabditis elegans infection model, we demonstrate that pathogen-induced neuronal signaling disrupts epidermal lysosomal activity and collagen remodeling.

Pathogen subversion of neuro-epidermal signaling impairs lysosomal function to disrupt collagen homeostasis in <i>Caenorhabditis elegans</i>
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by Qian Li, Yating Liu, Hanyi Chen, Weilie Xiao, Bin Qi The epidermis relies on collagen-rich extracellular matrices (ECMs) to maintain barrier integrity against pathogens.

Using Pseudomonas aeruginosa PA14- Caenorhabditis elegans infection model, we demonstrate that pathogen-induced neuronal signaling disrupts epidermal lysosomal activity and collagen remodeling.

This disruption leads to disorganized collagen structure, compromising cuticle integrity and host resistance.

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The useful part

by Qian Li, Yating Liu, Hanyi Chen, Weilie Xiao, Bin Qi The epidermis relies on collagen-rich extracellular matrices (ECMs) to maintain barrier integrity against pathogens. Using Pseudomonas aeruginosa PA14- Caenorhabditis elegans infection model, we demonstrate that pathogen-induced neuronal signaling disrupts epidermal lysosomal activity and collagen remodeling. This disruption leads to disorganized collagen structure, compromising cuticle integrity and host resistance.

How it works

  • NSIF-1 inhibits ELT-3 nuclear localization, blocking its role in lysosomal-dependent ECM repair.

Details worth keeping

PA14 infection triggers neurons to secrete NSIF-1 (Neuronal Secreted Immune Factor 1), which translocates to the epidermis and impairs lysosomal acidification, maturation, and degradation by suppressing the transcription factor ELT-3.

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