Neutrophil elastase-mediated increase in airway temperature during inflammation.
- Schmidt A Institute of Medical Microbiology and Hygiene, German Center for Infection Research, University Clinic Tübingen, Germany.
- Belaaouaj A INSERM U-1111, Centre International de Recherche en Infectiologie (CIRI), Lyon, France.
- Bissinger R Institute of Medical Microbiology and Hygiene, German Center for Infection Research, University Clinic Tübingen, Germany.
- Koller G King's College, London, England.
- Malleret L INSERM U-1111, Centre International de Recherche en Infectiologie (CIRI), Lyon, France.
- D'Orazio C Department of Pediatrics, Verona, Italy.
- Facchinelli M Ospedale Civile Maggiore, Verona, Italy.
- Schulte-Hubbert B Medical Clinic und Policlinic I Pneumology, Technical University Dresden, Dresden, Germany.
- Molinaro A Department of Chemical Sciences, Università di Napoli Federico II, Italy.
- Holst O Research Center Borstel, Center for Medicine and Biosciences, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
- Hammermann J Department of Pediatrics, Technical University Dresden, Dresden, Germany.
- Schniederjans M Helmholtz-Centre for Infection Research, Braunschweig, Germany.
- Meyer KC University of Wisconsin School of Medicine, Madison, USA.
- Damkiaer S Department of Systems Biology and Center for Biosustainability, Technical University of Denmark, Lyngby, Denmark.
- Piacentini G Ospedale Civile Maggiore, Verona, Italy.
- Assael B Department of Pediatrics, Verona, Italy.
- Bruce K King's College, London, England.
- Häußler S Research Center Borstel, Center for Medicine and Biosciences, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
- LiPuma JJ Department of Paediatrics, University of Michigan, Ann Arbor, USA.
- Seelig J Biophysical Chemistry, University of Basel, Basel Switzerland.
- Worlitzsch D Institute of Hygiene, University of Halle, Germany. Electronic address: dieter.worlitzsch@uk-halle.de.
- Döring G Institute of Medical Microbiology and Hygiene, German Center for Infection Research, University Clinic Tübingen, Germany.
- 2014-04-10
Published in:
- Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society. - 2014
Inflammation
Neutrophil elastase
Pseudomonas aeruginosa
Temperature
Adolescent
Animals
Body Temperature
Case-Control Studies
Child
Cystic Fibrosis
Disease Models, Animal
Female
Hot Temperature
Humans
Leukocyte Elastase
Male
Mice
Mice, Inbred C57BL
Pseudomonas Infections
Pseudomonas aeruginosa
Respiratory Tract Infections
English
BACKGROUND
How elevated temperature is generated during airway infections represents a hitherto unresolved physiological question. We hypothesized that innate immune defence mechanisms would increase luminal airway temperature during pulmonary infection.
METHODS
We determined the temperature in the exhaled air of cystic fibrosis (CF) patients. To further test our hypothesis, a pouch inflammatory model using neutrophil elastase-deficient mice was employed. Next, the impact of temperature changes on the dominant CF pathogen Pseudomonas aeruginosa growth was tested by plating method and RNAseq.
RESULTS
Here we show a temperature of ~38°C in neutrophil-dominated mucus plugs of chronically infected CF patients and implicate neutrophil elastase:α1-proteinase inhibitor complex formation as a relevant mechanism for the local temperature rise. Gene expression of the main pathogen in CF, P. aeruginosa, under anaerobic conditions at 38°C vs 30°C revealed increased virulence traits and characteristic cell wall changes.
CONCLUSION
Neutrophil elastase mediates increase in airway temperature, which may contribute to P. aeruginosa selection during the course of chronic infection in CF.
How elevated temperature is generated during airway infections represents a hitherto unresolved physiological question. We hypothesized that innate immune defence mechanisms would increase luminal airway temperature during pulmonary infection.
METHODS
We determined the temperature in the exhaled air of cystic fibrosis (CF) patients. To further test our hypothesis, a pouch inflammatory model using neutrophil elastase-deficient mice was employed. Next, the impact of temperature changes on the dominant CF pathogen Pseudomonas aeruginosa growth was tested by plating method and RNAseq.
RESULTS
Here we show a temperature of ~38°C in neutrophil-dominated mucus plugs of chronically infected CF patients and implicate neutrophil elastase:α1-proteinase inhibitor complex formation as a relevant mechanism for the local temperature rise. Gene expression of the main pathogen in CF, P. aeruginosa, under anaerobic conditions at 38°C vs 30°C revealed increased virulence traits and characteristic cell wall changes.
CONCLUSION
Neutrophil elastase mediates increase in airway temperature, which may contribute to P. aeruginosa selection during the course of chronic infection in CF.
- Language
-
- English
- Open access status
- bronze
- Identifiers
-
- DOI 10.1016/j.jcf.2014.03.004
- PMID 24713593
- Persistent URL
- https://sonar.ch/global/documents/232267
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