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Inflammasomes in respiratory disease: from bench to bedside

Guy Brusselle (UGent) , Sharen Provoost (UGent) , Ken Bracke (UGent) , Anna Kuchmiy (UGent) and Mohamed Lamkanfi (UGent)
(2014) CHEST. 145(5). p.1121-1133
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Abstract
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-1 beta and IL-18. Here, we summarize and review the inflammasome and its downstream effectors as therapeutic targets for the treatment of respiratory diseases.
Keywords
NALP3 INFLAMMASOME, CASPASE-1 ACTIVATION, MYCOBACTERIUM-TUBERCULOSIS, HOST-DEFENSE, NLRP3 INFLAMMASOME, OBSTRUCTIVE PULMONARY-DISEASE, INTERLEUKIN-1 RECEPTOR ANTAGONIST, RHEUMATOID-ARTHRITIS, AIM2 INFLAMMASOME, PARTICULATE MATTER

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Citation

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MLA
Brusselle, Guy, et al. “Inflammasomes in Respiratory Disease: From Bench to Bedside.” CHEST, vol. 145, no. 5, 2014, pp. 1121–33, doi:10.1378/chest.13-1885.
APA
Brusselle, G., Provoost, S., Bracke, K., Kuchmiy, A., & Lamkanfi, M. (2014). Inflammasomes in respiratory disease: from bench to bedside. CHEST, 145(5), 1121–1133. https://doi.org/10.1378/chest.13-1885
Chicago author-date
Brusselle, Guy, Sharen Provoost, Ken Bracke, Anna Kuchmiy, and Mohamed Lamkanfi. 2014. “Inflammasomes in Respiratory Disease: From Bench to Bedside.” CHEST 145 (5): 1121–33. https://doi.org/10.1378/chest.13-1885.
Chicago author-date (all authors)
Brusselle, Guy, Sharen Provoost, Ken Bracke, Anna Kuchmiy, and Mohamed Lamkanfi. 2014. “Inflammasomes in Respiratory Disease: From Bench to Bedside.” CHEST 145 (5): 1121–1133. doi:10.1378/chest.13-1885.
Vancouver
1.
Brusselle G, Provoost S, Bracke K, Kuchmiy A, Lamkanfi M. Inflammasomes in respiratory disease: from bench to bedside. CHEST. 2014;145(5):1121–33.
IEEE
[1]
G. Brusselle, S. Provoost, K. Bracke, A. Kuchmiy, and M. Lamkanfi, “Inflammasomes in respiratory disease: from bench to bedside,” CHEST, vol. 145, no. 5, pp. 1121–1133, 2014.
@article{4431529,
  abstract     = {{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-1 beta and IL-18. Here, we summarize and review the inflammasome and its downstream effectors as therapeutic targets for the treatment of respiratory diseases.}},
  author       = {{Brusselle, Guy and Provoost, Sharen and Bracke, Ken and Kuchmiy, Anna and Lamkanfi, Mohamed}},
  issn         = {{0012-3692}},
  journal      = {{CHEST}},
  keywords     = {{NALP3 INFLAMMASOME,CASPASE-1 ACTIVATION,MYCOBACTERIUM-TUBERCULOSIS,HOST-DEFENSE,NLRP3 INFLAMMASOME,OBSTRUCTIVE PULMONARY-DISEASE,INTERLEUKIN-1 RECEPTOR ANTAGONIST,RHEUMATOID-ARTHRITIS,AIM2 INFLAMMASOME,PARTICULATE MATTER}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{1121--1133}},
  title        = {{Inflammasomes in respiratory disease: from bench to bedside}},
  url          = {{http://doi.org/10.1378/chest.13-1885}},
  volume       = {{145}},
  year         = {{2014}},
}
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