ArticleParticle and fibre toxicology2025
Inhibition of protease-activated receptor-2 attenuates multi-walled carbon nanotube exacerbation of allergic lung disease in mice.
Article in Particle and fibre toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Role of the protease-activated receptor 2 in multi-walled carbon nanotube-induced macrophage polarizationFrontiers in toxicology · 2026Article
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4 authors.
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Abstract
backgroundOur previous work showed that exposure to multi-walled carbon nanotubes (MWCNTs) exacerbates allergic lung disease in mice induced by house dust mite extract (HDME). Furthermore, mice genetically deficient in the proteinase-activated receptor 2 (PAR2) exhibited reduced airway fibrosis after co-exposure to MWCNTs and HDME. The objective of this study was to determine whether inhibition of PAR2 signaling, using the monoclonal antibody SAM-11, attenuates MWCNT exacerbation of HDME-induced allergic lung disease.
methodsC57BL/6J mice were exposed to MWCNTs in the presence or absence of HDME via oropharyngeal aspiration over a 21-day protocol. SAM-11 or isotype control antibodies were administered prior to exposure. Bronchoalveolar lavage fluid (BALF) and lung tissue were analyzed for markers of allergic inflammation, airway remodeling, and fibrosis.
resultsSAM-11 treatment significantly reduced airway collagen deposition, eosinophilic inflammation, mucous cell metaplasia, and CD3
conclusionInhibition of canonical PAR2 signaling using SAM-11 attenuates multiple features of MWCNT-enhanced allergic lung disease with broader efficacy than PAR2-deficient models. These findings highlight PAR2 as a viable therapeutic target in allergic lung disease and asthma, suggesting that antibody-based blockade is a promising strategy for mitigating allergen and particle-induced disease.
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