Neutrophil elastase-mediated increase in airway temperature during inflammation

Research output: Contribution to journalJournal article – Annual report year: 2014Researchpeer-review

  • Author: Schmidt, Annika

    University Clinic Tübingen, Germany

  • Author: Belaaouaj, Azzaq

    Centre International de Recherche en Infectiologie, France

  • Author: Bissinger, Rosi

    University Clinic Tübingen, Germany

  • Author: Koller, Garrit

    King’s College London, United Kingdom

  • Author: Malleret, Laurette

    Centre International de Recherche en Infectiologie, France

  • Author: D'Orazio, Ciro

    Verona University Hospital, Italy

  • Author: Facchinelli, Martino

    Ospedale Civile Maggiore, Verona, Italy

  • Author: Schulte-Hubbert, Bernhard

    Dresden University of Technology, Germany

  • Author: Molinaro, Antonio

    University of Naples Federico II, Italy

  • Author: Holst, Otto

    Airway Research Center North , Germany

  • Author: Hammermann, Jutta

  • Author: Schniederjans, Monika

  • Author: Meyer, Keith C.

  • Author: Pedersen, Søren Damkiær

    Center for Systems Microbiology, Department of Systems Biology, Technical University of Denmark

  • Author: Piacentini, Giorgio

  • Author: Assael, Baroukh

  • Author: Bruce, Kenneth

  • Author: Häußler, Susanne

  • Author: LiPuma, John J.

  • Author: Seelig, Joachim

  • Author: Worlitzsch, Dieter

  • Author: Döring, Gerd

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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.
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.
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.
Neutrophil elastase mediates increase in airway temperature, which may contribute to P. aeruginosa selection during the course of chronic infection in CF.
Original languageEnglish
JournalJournal of Cystic Fibrosis
Issue number6
Pages (from-to)623-631
Publication statusPublished - 2014
CitationsWeb of Science® Times Cited: No match on DOI

ID: 103084102