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CARMA3 Mediates Allergic Lung Inflammation in Response to Alternaria alternata
Journal article   Open access   Peer reviewed

CARMA3 Mediates Allergic Lung Inflammation in Response to Alternaria alternata

Benjamin Causton, Ana Pardo-Saganta, Jacob Gillis, Katherine Discipio, Tristan Kooistra, Jayaraj Rajagopal, Ramnik J Xavier, Josalyn L Cho and Benjamin D Medoff
American journal of respiratory cell and molecular biology, Vol.59(6), pp.684-694
12/2018
DOI: 10.1165/rcmb.2017-0181OC
PMCID: PMC6293075
PMID: 29958012
url
https://doi.org/10.1165/rcmb.2017-0181OCView
Published (Version of record) Open Access

Abstract

The airway epithelial cell (AEC) response to allergens helps initiate and propagate allergic inflammation in asthma. CARMA3 is a scaffold protein that mediates G protein-coupled receptor-induced NF-κB activation in airway epithelium. In this study, we demonstrate that mice with CARMA3-deficient AECs have reduced airway inflammation, as well as reduced type 2 cytokine levels in response to Alternaria alternata. These mice also have reduced production of IL-33 and IL-25, and reduced numbers of innate lymphoid cells in the lung. We also show that CARMA3-deficient human AECs have decreased production of proasthmatic mediators in response to A. alternata. Finally, we show that CARMA3 interacts with inositol 1,4,5-trisphosphate receptors in AECs, and that inhibition of CARMA3 signaling reduces A. alternata-induced intracellular calcium release. In conclusion, we show that CARMA3 signaling in AECs helps mediate A. alternata-induced allergic airway inflammation, and that CARMA3 is an important signaling molecule for type 2 immune responses in the lung.

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