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Inflammasomes in Respiratory DiseaseInflammasomes in Lung Disease: From Bench to Bedside

Guy G. Brusselle, MD, PhD; Sharen Provoost, PhD; Ken R. Bracke, PhD; Anna Kuchmiy, PhD; Mohamed Lamkanfi, PhD
Author and Funding Information

From the Laboratory for Translational Research of Obstructive Pulmonary Disease (Drs Brusselle, Provoost, and Bracke), Ghent University Hospital, Ghent, Belgium; the Departments of Epidemiology and Respiratory Medicine (Dr Brusselle), Erasmus MC, Rotterdam, The Netherlands; the Department of Medical Protein Research (Drs Kuchmiy and Lamkanfi), Flanders Institute for Biotechnology (VIB), Ghent, Belgium; and the Department of Biochemistry (Drs Kuchmiy and Lamkanfi), Ghent University, Ghent, Belgium.

Correspondence to: Guy G. Brusselle, MD, PhD, Laboratory for Translational Research of Obstructive Pulmonary Disease, Ghent University, De Pintelaan 185, B-9000 Ghent, Belgium; e-mail: guy.brusselle@ugent.be


Funding/Support: Work in Dr Lamkanfi’s laboratory is supported in part by the European Union [Marie-Curie Grant 256432], European Research Council [Grant 281600], and the Fund for Scientific Research Flanders (FWO) [Grants G030212N, 1.2.201.10.N.00, and 1.5.122.11.N.00]. Drs Provoost and Bracke are postdoctoral researchers of FWO. Presented work within the Department of Respiratory Medicine of Ghent University is funded by grants from the FWO, the Concerted Action of Ghent University, and the Interuniversity Attraction Poles Program.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;145(5):1121-1133. doi:10.1378/chest.13-1885
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The respiratory tract of human subjects is constantly exposed to harmful microbes and air pollutants. The immune system responds to these offenders to protect the host, but an unbalanced inflammatory response itself may promote tissue damage and ultimately lead to acute and chronic respiratory diseases. Deregulated inflammasome activation is emerging as a key modulator of respiratory infections and pathologic airway inflammation in patients with asthma, COPD, and pulmonary fibrosis. Assembly of these intracellular danger sensors in cells of the respiratory mucosa and alveolar compartment triggers a proinflammatory cell death mode termed pyroptosis and leads to secretion of bioactive IL-1β and IL-18. Here, we summarize and review the inflammasome and its downstream effectors as therapeutic targets for the treatment of respiratory diseases.

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