Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
 free
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
 free
 free
 
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve
Pubget Overpricing |  
lüll
Apoptotic cell clearance by bronchial epithelial cells critically influences airway inflammation Juncadella IJ; Kadl A; Sharma AK; Shim YM; Hochreiter-Hufford A; Borish L; Ravichandran KSNature 2013[Jan]; 493 (7433): 547-51Lung epithelial cells can influence immune responses to airway allergens. Airway epithelial cells also undergo apoptosis after encountering environmental allergens; yet, relatively little is known about how these are cleared, and their effect on airway inflammation. Here we show that airway epithelial cells efficiently engulf apoptotic epithelial cells and secrete anti-inflammatory cytokines, dependent upon intracellular signalling by the small GTPase Rac1. Inducible deletion of Rac1 expression specifically in airway epithelial cells in a mouse model resulted in defective engulfment by epithelial cells and aberrant anti-inflammatory cytokine production. Intranasal priming and challenge of these mice with house dust mite extract or ovalbumin as allergens led to exacerbated inflammation, augmented Th2 cytokines and airway hyper-responsiveness, with decreased interleukin (IL)-10 in bronchial lavages. Rac1-deficient epithelial cells produced much higher IL-33 upon allergen or apoptotic cell encounter, with increased numbers of nuocyte-like cells. Administration of exogenous IL-10 'rescued' the airway inflammation phenotype in Rac1-deficient mice, with decreased IL-33. Collectively, these genetic and functional studies suggest a new role for Rac1-dependent engulfment by airway epithelial cells and in establishing the anti-inflammatory environment, and that defects in cell clearance in the airways could contribute to inflammatory responses towards common allergens.|*Apoptosis[MESH]|*Phagocytosis[MESH]|Allergens/immunology[MESH]|Animals[MESH]|Bronchi/*cytology/immunology/pathology[MESH]|Bronchoalveolar Lavage Fluid/chemistry/immunology[MESH]|Dust/immunology[MESH]|Epithelial Cells/immunology/*physiology[MESH]|Immunity, Innate/immunology[MESH]|Inflammation/immunology/*pathology[MESH]|Interleukin-10/biosynthesis/immunology[MESH]|Interleukin-33[MESH]|Interleukins/biosynthesis/immunology[MESH]|Lung/immunology/*pathology[MESH]|Mice[MESH]|Ovalbumin/immunology[MESH]|Pyroglyphidae/immunology[MESH]|Respiratory Hypersensitivity/immunology/*pathology[MESH]|Th2 Cells/immunology/metabolism[MESH]|Up-Regulation[MESH]|rac1 GTP-Binding Protein/deficiency/genetics/metabolism[MESH] |
