APA
Click to copy
Joulia, R., Puttur, F., Stölting, H., Traves, W. J., Entwistle, L. J., Voitovich, A., … Lloyd, C. M. (2024). Mast cell activation disrupts interactions between endothelial cells and pericytes during early life allergic asthma. The Journal of Clinical Investigation, 134, e173676. https://doi.org/10.1172/JCI173676
Chicago/Turabian
Click to copy
Joulia, Régis, Franz Puttur, Helen Stölting, William J. Traves, Lewis J. Entwistle, Anastasia Voitovich, Minerva Garcia Martín, et al. “Mast Cell Activation Disrupts Interactions between Endothelial Cells and Pericytes during Early Life Allergic Asthma.” The Journal of Clinical Investigation 134 (2024): e173676.
MLA
Click to copy
Joulia, Régis, et al. “Mast Cell Activation Disrupts Interactions between Endothelial Cells and Pericytes during Early Life Allergic Asthma.” The Journal of Clinical Investigation, vol. 134, 2024, p. e173676, doi:10.1172/JCI173676.
BibTeX Click to copy
@article{joulia2024a,
title = {Mast cell activation disrupts interactions between endothelial cells and pericytes during early life allergic asthma},
year = {2024},
journal = {The Journal of Clinical Investigation},
pages = {e173676},
volume = {134},
doi = {10.1172/JCI173676},
author = {Joulia, Régis and Puttur, Franz and Stölting, Helen and Traves, William J. and Entwistle, Lewis J. and Voitovich, Anastasia and Martín, Minerva Garcia and Al-Sahaf, May and Bonner, Katie and Scotney, Elizabeth and Molyneaux, Philip L. and Hewitt, Richard J. and Walker, Simone A. and Yates, Laura and Saglani, Sejal and Lloyd, Clare M.}
}
Allergic asthma generally starts during early life and is linked to substantial tissue remodelling and lung dysfunction. Although angiogenesis is a feature of the disrupted airway, the impact of allergic asthma on the pulmonary microcirculation during early life is unknown. Here, using quantitative imaging in precision-cut lung slices (PCLS), we report that exposure of neonatal mice to house dust mite (HDM) extract disrupts endothelial cell/pericyte interactions in adventitial areas. Central to the blood vessel structure, the loss of pericyte coverage was driven by mast cell (MCs) proteases, such as tryptase, that can induce pericyte retraction and loss of the critical adhesion molecule N-Cadherin. Furthermore, spatial transcriptomics of paediatric asthmatic endobronchial biopsies suggests intense vascular stress and remodelling linked with increased expression of MC activation pathways in regions enriched in blood vessels. These data provide previously unappreciated insights into the pathophysiology of allergic asthma with potential long-term vascular defects.