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NK cells and Lipoxin A4 promote resolution of eosinophilic inflammation after nasal allergen challenge
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  • Anh Poirot,
  • Guillaume Wacht,
  • Lehalle Christine,
  • Philippe Saas,
  • Nelly Frossard,
  • Bernard Geny,
  • Frederic de Blay,
  • Cindy Barnig
Anh Poirot
Hopitaux universitaires de Strasbourg
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Guillaume Wacht
EA 3072, University of Strasbourg
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Lehalle Christine
UMR 7200 CNRS / Université de Strasbourg, Laboratoire d’Innovation Thérapeutique and LabEx MEDALIS, Faculté de Pharmacie
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Philippe Saas
Univ. Bourgogne Franche-Comté, INSERM, EFS BFC, UMR1098, Interactions Hôte-Greffon-Tumeur/Ingénierie Cellulaire et Génique, LabEx LipSTIC
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Nelly Frossard
CNRS-Université de Strasbourg and LabEx Medalis, Faculté de Pharmacie
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Bernard Geny
Hôpitaux Universitaires de Strasbourg
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Frederic de Blay
Department of Chest Disease, University Hospital of Strasbourg
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Cindy Barnig
University Hospital Centre Besancon
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Background: Resolution of inflammation is now recognized as a tightly regulated and active process. Lipoxins (LX) are lead members of a larger family of specialized pro-resolving mediators with unique anti-inflammatory and pro-resolving properties. Recent studies implicated natural killer (NK) cells in the resolution of allergic airway inflammation, notably in promoting eosinophil apoptosis. The aim of the study was to better understand the pro-resolving actions of NK cells and LXA4 during allergic eosinophilic airway inflammation. Methods: 20 subjects with grass pollen allergic rhinitis were included. A nasal provocation test with either a single grass pollen allergen threshold dose or diluent was used. Nasal lavage fluid and cells were collected at baseline and at different time points after challenge. For in vitro assays, eosinophils were incubated with NK cells. Results: We observed that NK cells were recruited to the nasal mucosa shortly after the initiation of the allergic inflammatory response. This recruitment correlated with eosinophilic inflammation. In vitro assays demonstrated that direct contact and a combined action of CD56bright and CD56dim NK cells were needed to promote autologous eosinophil apoptosis. We furthermore observed that local LXA4 production correlated with the peak of neutrophil nasal mucosal infiltration, suggesting a potential role of neutrophils in LXA4 biosynthesis during the early phase of the allergic inflammatory response. Last, LXA4 appeared as essential to inhibit the in vitro release of eosinophil superoxide triggered by NK cells. Conclusion: Together, these findings indicate a synergistic role for NK cells and LXA4 in the resolution of allergic eosinophilic inflammation.