IL-17 and TNF-alpha are essential mediators of M. catarrhalis triggered exacerbation of HDM allergic airway inflammation
In this study we have demonstrated in a murine model of allergic airway inflammation that intranasal infection with the human pathogen M. catarrhalis exacerbate pulmonary inflammation. The aim of the study was: i) to establish an animal model of infection induced exacerbation of lung allergic re...
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|Summary:||In this study we have demonstrated in a murine model of allergic airway inflammation that
intranasal infection with the human pathogen M. catarrhalis exacerbate pulmonary
The aim of the study was: i) to establish an animal model of infection induced exacerbation of
lung allergic reactions, ii) to study the pulmonary immune responses of HDM allergic animals
with and without infection and iii) to identify potential targets to prevent exacerbation of lung
The essential findings are that the human pathogen, M. catarrhalis, is able to colonize murine
lungs for approximately 6 days and thus can be used as a model germ for acute respiratory
infection. We further could show, that infection with M. catarrhalis exacerbates allergic
airway inflammation (AAI) via innate and adaptive immune responses, depending on the time
of infection, i.e. before, during or after established allergic sensitization. While M. catarrhalis
infection in a non-allergic environment induced high amounts of IL-6 and TNF- but
moderate amounts of T cell derived IFN- and IL-17, infection triggered exacerbation of AAI
mainly by IL-17 and TNF- but not IL-6.
Further, we could show that lack of IL-17 or neutralization of TNF- but not IL-6 is able to
prevent M. catarrhalis induced exacerbation of AAI.
In conclusion, infection with M. catarrhalis has the potential to exacerbate allergic airway
inflammation at any time of infection and temporary treatment with anti-IL-17 and/or anti-
TNF-antibodies may be appropriate to prevent aggravation of this lung disease.|