Activities per year
Objectives: To identify the cellular source and the role of IL17A in the early phase of lung injury
Methods: Lung injury was induced in WT (C57BL/6) and IL-17 KO mice with aerosolised LPS (100 µg) or Pseudomonas aeruginosa infection. Detailed phenotyping of the cells expressing RORγt, the transcriptional regulator of IL-17 production, in the mouse lung at 24 hours was carried out by flow cytometry.
Measurement and Main Results: A 100-fold reduction in neutrophil infiltration was observed in the lungs of the IL-17A KO compared to wild type (WT) mice. The majority of RORγt+ cells in the mouse lung were the recently identified type 3 innate lymphoid cells (ILC3). Detailed characterisation revealed these pulmonary ILC3s (pILC3s) to be discrete from those described in the gut. The critical role of these cells was verified by inducing injury in Rag2 KO mice which lack T cells but retain ILCs. No amelioration of pathology was observed in the Rag2 KO mice.
Conclusions: IL-17 is rapidly produced during lung injury and significantly contributes to early immunopathogenesis. This is orchestrated largely by a distinct population of pILC3 cells. Modulation of pILC3s’ activity may potentiate early control of the inflammatory dysregulation seen in ARDS, opening up new therapeutic targets.
|Number of pages||9|
|Journal||American Journal of Respiratory and Critical Care Medicine|
|Early online date||21 Dec 2015|
|Publication status||Published - 15 Feb 2016|
- ARDS, acute lung injury, IL-17, lymphocyte, ILC3, pILC
Beckie Ingram (Speaker)09 Feb 2016
Activity: Talk or presentation types › Invited talk
Beckie Ingram (Participant)2013 → …
Activity: Participating in or organising an event types › Participation in conference