2026-10-13T07:45:45Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33968025 2026-09-22T17:39:43Z category_146 category_7 category_8 category_12 category_14 category_15 category_21 category_272 category_46 category_734 category_122 category_132 category_134 portal_5 item_type_3 month_year_09_2026

<p>Oligonucleotide primers used in this study.</p> Qian Li (114642) Yating Liu (1731835) Hanyi Chen (4855570) Weilie Xiao (2735008) Bin Qi (495384) Space Science Medicine Microbiology Cell Biology Molecular Biology Neuroscience Biotechnology Environmental Sciences not elsewhere classified Immunology Biological Sciences not elsewhere classified Mental Health Infectious Diseases Virology rich extracellular matrices maintain barrier integrity div >< p dependent ecm repair compromising cuticle integrity pseudomonas aeruginosa </ caenorhabditis elegans </ restores lysosomal function impairs lysosomal acidification disrupt lysosomal function transcription factor elt infection remains unclear enhances collagen density disorganized collagen structure disrupt collagen homeostasis 3 nuclear localization 1 inhibits elt collagen homeostasis 1 </ infection model counteract infection collagen remodeling collagen organization study reveals potential targets pa14 -< neuronal origin knockdown confirms improves survival host resistance genetic mutation disruption leads <div><p>The epidermis relies on collagen-rich extracellular matrices (ECMs) to maintain barrier integrity against pathogens. Lysosomes regulate cuticle collagen turnover, yet how neuronal signaling modulates epidermal lysosomal function and collagen organization during infection remains unclear. Using <i>Pseudomonas aeruginosa</i> PA14-<i>Caenorhabditis elegans</i> infection model, we demonstrate that pathogen-induced neuronal signaling disrupts epidermal lysosomal activity and collagen remodeling. 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. This disruption leads to disorganized collagen structure, compromising cuticle integrity and host resistance. Genetic mutation of <i>nsif-1</i> restores lysosomal function, enhances collagen density, and improves survival, while neuron-specific <i>nsif-1</i> knockdown confirms its neuronal origin. Moreover, NSIF-1 inhibits ELT-3 nuclear localization, blocking its role in lysosomal-dependent ECM repair. Our study reveals a neuro-epidermal axis wherein pathogens exploit neuronal signals to disrupt lysosomal function and collagen homeostasis, identifying NSIF-1 and ELT-3 as potential targets to counteract infection-driven ECM dysregulation.</p></div> 2026-09-22T18:00:57Z Dataset Dataset 10.1371/journal.pbio.3004016.s026 https://figshare.com/articles/dataset/_p_Oligonucleotide_primers_used_in_this_study_p_/33968025 CC BY 4.0