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

Triantafilou K, Kar S, van Kuppeveld FJ, Triantafilou M.

Am J Respir Cell Mol Biol. 2013 Dec;49(6):923-34.

 

Cardiff University, Institute of Infection and Immunity, Department of Child Health, School of Medicine, University Hospital of Wales, Heath Park, Cardiff, Wales; and

Department of Medical Microbiology, Nijmegen Center for Molecular Life Sciences, University Medical Center Nijmegen, Nijmegen, The Netherlands

 

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 NLRC5inflammasome activation and IL-1{Beta} secretion in bronchial cells. 2B protein targets the endoplasmic reticulum and Golgi and induces Ca(2+) 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 Ca(2+) fluxes and trigger IL-1{Beta} secretion. These results reveal for the first time that human rhinovirus infection in primary bronchial cells triggers inflammasome activation.

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