Guest guest Posted September 3, 2011 Report Share Posted September 3, 2011 This article is interesting because it shows that the lungs can interact at a distance with the bone marrow to modulate the patient's immune response. This is precisely the kind of thing that is happening in Samter's.It also shows how trying to shift the Th2 immune biais associated with AERD/asthma/chronic sinusitis more towards Th1 might be beneficial.-----------J Immunol. 2011 Aug 26. [Epub ahead of print]IFN-{gamma} Acts on the Airway Epithelium To Inhibit Local and Systemic Pathology in Allergic Airway Disease. C, Provost K, Niu N, Homer R, Cohn L.SourceSection of Pulmonary and Critical Care, Yale University School of Medicine, New Haven, CT 06520.AbstractInhibiting allergic airway inflammation is the goal of therapy in persistent asthma. Administration of medication via the airways delivers drug directly to the site of inflammation and avoids systemic side effects but often fails to modulate systemic features of asthma. We have shown that Th1 cells, through production of IFN-γ, inhibit many Th2-induced effector functions that promote disease. Using a newly generated mouse that expresses IFN-γR only on airway epithelial cells, we show that the airway epithelium controls a range of pathological responses in asthma. IFN-γ acting only through the airway epithelium inhibits mucus, chitinases, and eosinophilia, independent of Th2 cell activation. IFN-γ signaling through the airway epithelium inhibits eosinophil generation in the bone marrow, indicating that signals on the airway mucosal surface can regulate distant functions to inhibit disease. IFN-γ actions through the airway epithelium will limit airway obstruction and inflammation and may be therapeutic in refractory asthma.PMID: 21873527 [PubMed - as supplied by publisher] Quote Link to comment Share on other sites More sharing options...
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