Journal
FRONTIERS IN IMMUNOLOGY
Volume 13, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2022.877383
Keywords
allergic asthma; Alt a 1; TLR4; alveolar macrophage; mouse model
Categories
Funding
- Spanish Ministry of Science and Innovation
- Spanish Ministry of Science and Innovation - Spanish Research State Agency [PID2020-113629RB00/AEI/10.13039/501100011033]
- European Commission [H2020-NMBP-X- KET-2017-768641]
- Universidad Politecnica de Madrid and Banco Santander
- Community of Madrid [S2018/BAA-4574]
- ESF
- ERDF RD
- Instituto de Salud Carlos III (ISCIII)
- FEDER Thematic Networks and Cooperative Research Centers: ARADYAL [RD16/0006/0003, RD16/0006/0013]
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This study demonstrated that Alt a 1 can induce asthmatic phenotypes in vivo, promoting tissue remodeling and infiltration of CD45+ cells, particularly eosinophils and macrophages (Siglec F+ and F4/80+). Furthermore, the study revealed that Alt a 1 sensitization is mediated by the TLR4-macrophage axis.
The mold Alternaria alternata is one of the main sources of asthma exacerbation, being its major allergen, Alt a 1, indispensable for its development. The main objective of this work was to answer two main questions: 1) can Alt a 1 by itself (without any other context) induce an asthmatic profile in vivo?; and 2) Which molecular mechanisms take place during this phenomenon? To answer both questions, we have developed a mouse model of allergic asthma using only Alt a 1 for mice sensitization. We also made use of in-vitro cellular models and computational studies to support some aspects of our hypothesis. Our results showed that Alt a 1 can induce an asthmatic phenotype, promoting tissue remodeling and infiltration of CD45+ cells, especially eosinophils and macrophages (Siglec F+ and F4/80+). Also, we have found that Alt a 1 sensitization is mediated by the TLR4-macrophage axis.
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