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J Cyst Fibros. 2014 Dec;13(6):623-31. doi: 10.1016/j.jcf.2014.03.004. Epub 2014 Apr 6.

Neutrophil elastase-mediated increase in airway temperature during inflammation.

Author information

1
Institute of Medical Microbiology and Hygiene, German Center for Infection Research, University Clinic Tübingen, Germany.
2
INSERM U-1111, Centre International de Recherche en Infectiologie (CIRI), Lyon, France.
3
King's College, London, England.
4
Department of Pediatrics, Verona, Italy.
5
Ospedale Civile Maggiore, Verona, Italy.
6
Medical Clinic und Policlinic I Pneumology, Technical University Dresden, Dresden, Germany.
7
Department of Chemical Sciences, Università di Napoli Federico II, Italy.
8
Research Center Borstel, Center for Medicine and Biosciences, Airway Research Center North (ARCN), Member of the German Center for Lung Research (DZL), Borstel, Germany.
9
Department of Pediatrics, Technical University Dresden, Dresden, Germany.
10
Helmholtz-Centre for Infection Research, Braunschweig, Germany.
11
University of Wisconsin School of Medicine, Madison, USA.
12
Department of Systems Biology and Center for Biosustainability, Technical University of Denmark, Lyngby, Denmark.
13
Department of Paediatrics, University of Michigan, Ann Arbor, USA.
14
Biophysical Chemistry, University of Basel, Basel Switzerland.
15
Institute of Hygiene, University of Halle, Germany. Electronic address: dieter.worlitzsch@uk-halle.de.

Abstract

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.

KEYWORDS:

Inflammation; Neutrophil elastase; Pseudomonas aeruginosa; Temperature

PMID:
24713593
DOI:
10.1016/j.jcf.2014.03.004
[Indexed for MEDLINE]
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