Tick extracellular vesicles impair epidermal homeostasis through immune-epithelial networks during hematophagy
Marnin, L.; Bogale, H.; Laukaitis-Yousey, H.; Valencia, L.; Rolandelli, A.; O'Neal, A.; Ferraz, C.; Schmitter-Sanchez, A.; Bencosme Cuevas, E.; Nguyen, T.-T.; Leal-Galvan, B.; Rickert, D.; Bruno, V. M.; Mendes, M. T.; Samaddar, S.; Butler, L. R.; Singh, N.; Cabrera Paz, F.; Oliver, J.; Jameson, J.; Munderloh, U.; Oliva Chavez, A.; Mulenga, A.; Park, S.; Serre, D.; Pedra, J. H. F.
10.1101/2023.11.10.566612 bioRxivShow abstract
Wound healing has been extensively studied through the lens of inflammatory disorders and cancer, but limited attention has been given to hematophagy and arthropod-borne diseases. Hematophagous ectoparasites, including ticks, subvert the wound healing response to maintain prolonged attachment and facilitate blood-feeding. Here, we unveil a strategy by which extracellular vesicles (EVs) ensure blood-feeding and arthropod survival in three medically relevant tick species. Through single cell RNA sequencing and murine genetics, we demonstrate that wildtype animals infested with EV-deficient Ixodes scapularis display a unique epidermal sub-population with a mesenchymal-like transcriptional program and an overrepresentation of pathways connected to wound healing. Furthermore, tick EVs inhibit proliferation and diminish the capacity of wound closure in keratinocytes. This occurrence was linked to phosphoinositide 3-kinase activity, keratinocyte growth factor 1 (KGF-1) and transforming growth factor {beta} (TGF-{beta}) levels. Collectively, we uncovered a strategy employed by a blood-feeding arthropod that disrupts the circuitry in cutaneous wound healing, contributing to ectoparasite fitness.
Matching journals
The top 4 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- ATF6 enables pathogen infection in ticks by inducing stomatin and altering cholesterol dynamics 96%
- Resistance to host antimicrobial peptides mediates resilience of gut commensals during infection and aging in Drosophila 95%
- Homeostatic, repertoire and transcriptional relationships between colon T regulatory cell subsets 94%
Similar papers in this journal
- Parasite-Induced IFN-g Regulates Host Defense via CD115 and mTOR-Dependent Mechanism of Tissue-Resident Macrophage Death 94%
- Exposure to mycobacterium remodels alveolar macrophages and the early innate response to Mycobacterium tuberculosis infection 94%
- Local association of Trypanosoma cruzi chronic infection foci and enteric neuropathic lesions at the tissue micro-domain scale 93%
Similar papers in this journal
- The pseudokinase Trib1 regulates the transition of exhausted T cells to a KLR+ CD8+ effector state and its deletion improves checkpoint blockade 94%
- Infection-Induced Elevation of Gut Glycosaminoglycans Fosters Microbiota Expansion in Drosophila melanogaster 94%
- MAIT cells protect against sterile lung injury 94%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.