BACKGROUND: @entity32 is dominated either by eosinophil and/or neutrophil accumulation in airways. Disposal of these inflammatory cells is the key to disease control. Eosinophilic @entity32 is responsive to @entity228 treatment, while neutrophilic @entity32 is resistant and increases the burden of global health care. @entity228 resistant @entity565 remains mechanistically poorly understood and requires novel effective therapeutic strategies. OBJECTIVE: We thought to explore the underlying mechanisms of @entity32 persistence as well as @entity228 resistance, and to investigate a new strategy of effective treatment against @entity228 -insensitive @entity565 . METHODS: @entity19 models of either @entity1712 -dominated or neutrophils-dominated @entity32 were used in this study to test @entity228 sensitivity in vivo and in vitro. We also used vav- @entity1379 @entity19 to confirm the importance of granulocytes apoptosis in the clearance of @entity32 . Finally, @entity1379 inhibitors @entity2427 or @entity35360 -were tested for their therapeutic effects against @entity1712 or neutrophilic @entity32 and airway hyperresponsiveness. RESULTS: Overexpression of @entity1379 protein was found to be responsible for persistence of granulocytes in bronchoalveolar lavage fluid following allergic challenge. This was important as allergen-induced @entity32 aggravated and persisted in vav- @entity1379 @entity19 , where nucleated hematopoietic cells were over-expressed with @entity1379 and resistant to apoptosis. @entity1379 inhibitors, @entity2427 or @entity35360 , play efficient roles in alleviation of either @entity1712 or @entity228 resistant-neutrophilic @entity32 , by inducing apoptosis of immune cell, such as @entity1712 , neutrophils, @entity61 , Th17 and dendritic cells. Moreover, these inhibitors were found to be more efficient than @entity479 to induce granulocytes apoptosis ex vivo from severe @entity565 @entity1 . CONCLUSION: Apoptosis of inflammatory cells is essential for the clearance of allergen-induced @entity32 . @entity1379 inhibitors @entity2427 or @entity35360 may be promising drugs for the treatment against @entity32 , especially for @entity228 -insensitive neutrophilic @entity32 .

XXXX Inhibitors Reduce @entity479 -insensitive Airway Inflammation.

@entity1712 :: ('MESH:D004802', 'Disease') :: ['eosinophilic', 'eosinophils'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation', 'airway inflammation', 'Asthmatic inflammation'] @entity1 :: ('9606', 'Species') :: ['patients'] @entity19 :: ('10090', 'Species') :: ['Mouse', 'transgenic mice'] @entity565 :: ('MESH:D001249', 'Disease') :: ['neutrophilic asthma', 'asthma'] @entity228 :: ('CHEBI:50858', 'Chemical') :: ['corticosteroid', 'Corticosteroid'] @entity61 :: ('15111(Tax:10090)', 'Gene') :: ['Th2'] @entity35360 :: ('MESH:C579720', 'Chemical') :: ['ABT-199'] @entity1379 :: ('12043(Tax:10090)', 'Gene') :: ['Bcl-2'] @entity2427 :: ('MESH:C501332', 'Chemical') :: ['ABT-737'] @entity479 :: ('D013256', 'Chemical') :: ['steroid']
@entity1379 :: (12043(Tax:10090),Gene) :: ['Bcl-2']
