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Am J Respir Cell Mol Biol. 2013 Dec;49(6):923-34. doi: 10.1165/rcmb.2013-0032OC.

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

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


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 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-1β secretion. These results reveal for the first time that human rhinovirus infection in primary bronchial cells triggers inflammasome activation.

[Indexed for MEDLINE]

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