Rhinovirus-induced calcium flux triggers NLRP3 and NLRC5 activation in bronchial cells

Triantafilou, Kathy ORCID: https://orcid.org/0000-0002-7473-6278, Kar, Satwik, van Kuppeveld, Frank J. M. and Triantafilou, Martha ORCID: https://orcid.org/0000-0002-7473-6278 2013. Rhinovirus-induced calcium flux triggers NLRP3 and NLRC5 activation in bronchial cells. American Journal of Respiratory Cell and Molecular Biology 49 (6) , p. 923. 10.1165/rcmb.2013-0032OC

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Abstract

Human rhinoviruses have been linked with underlying lung disorders, such as asthma and chronic obstructive pulmonary disease, in children and adults. However, the mechanism of virus-induced airway inflammation is poorly understood. In this study, using virus deletion mutants and silencing for nucleotide-binding oligomerization domain–like receptors (NLRs), we show that the rhinovirus ion channel protein 2B triggers NLRP3 and NLRC5 inflammasome activation and IL-1β secretion in bronchial cells. 2B protein targets the endoplasmic reticulum and Golgi and induces Ca2+ reduction in these organelles, thereby disturbing the intracellular calcium homeostasis. NLRP3 and NLRC5 act in a cooperative manner during the inflammasome assembly by sensing intracellular Ca2+ fluxes and trigger IL-1β secretion. These results reveal for the first time that human rhinovirus infection in primary bronchial cells triggers inflammasome activation.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Medicine
Publisher:	American Thoracic Society
ISSN:	1044-1549
Date of Acceptance:	10 June 2013
Last Modified:	24 Oct 2022 07:37
URI:	https://orca.cardiff.ac.uk/id/eprint/115428

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