Neutrophil elastase-mediated increase in airway temperature during inflammation

Annika Schmidt, Azzaq Belaaouaj, Rosi Bissinger, Garrit Koller, Laurette Malleret, Ciro D'Orazio, Martino Facchinelli, Bernhard Schulte-Hubbert, Antonio Molinaro, Otto Holst, Jutta Hammermann, Monika Schniederjans, Keith C. Meyer, Søren Damkiær Pedersen, Giorgio Piacentini, Baroukh Assael, Kenneth Bruce, Susanne Häußler, John J. LiPuma, Joachim SeeligDieter Worlitzsch, Gerd Döring

    Research output: Contribution to journalJournal articleResearchpeer-review


    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


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