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• W2022338923 abstract "PurposeLong term survival after lung transplantation (LTx) is restricted by the development of chronic lung allograft dysfunction (CLAD). CLAD represents at least 2 sub-phenotypes: restrictive allograft syndrome (RAS) and bronchiolitis obliterans syndrome (BOS), of which the exact pathophysiology remain elusive. A previous study demonstrated that increased broncho-alveolar lavage eosinophilia predisposed to CLAD. We further investigated the presence of eosinophils in explants lung tissue of CLAD.MethodsSections of BOS (n=16) and RAS (n=16) lungs were stained and quantified compared to (non-transplant) control lungs (n=20). Eosinophils, identified by the marker EG2, were counted in three different compartments; around the airway, in the parenchyma and around the blood vessel. Results were represented as the mean number (±SEM) of cells per high power field.ResultsRepresentative staining of BOS (A), RAS (B) and control (C) are provided in figure 1. Around the airways, eosinophils were significantly increased in BOS (16.7±4.8; p<0.05) and in RAS (13.4±4.0; p<0.05) compared to control (2.8±0.8). In the parenchyma, there were more eosinophils present in BOS (8.8±1.4; p<0.05), but not in RAS (8.2±2.2), compared to control (3.9±0.9). Around the blood vessels, both BOS (11.4±2.1; p<0.01) and RAS (9.8±1.9; p<0.05) demonstrated an increased number of eosinophils compared to control (4.0±0.6). The number of eosinophils around the airways correlated with eosinophil numbers in the parenchyma (R=0.55, p<0.0001) and around the blood vessels (R=0.79, p<0.0001).ConclusionEosinophils, regulated by a Th2 immune response, are increased in BOS and RAS which may implicate a new pathway. These findings may lead to additional therapeutic options to improve outcome after LTx in the future. PurposeLong term survival after lung transplantation (LTx) is restricted by the development of chronic lung allograft dysfunction (CLAD). CLAD represents at least 2 sub-phenotypes: restrictive allograft syndrome (RAS) and bronchiolitis obliterans syndrome (BOS), of which the exact pathophysiology remain elusive. A previous study demonstrated that increased broncho-alveolar lavage eosinophilia predisposed to CLAD. We further investigated the presence of eosinophils in explants lung tissue of CLAD. Long term survival after lung transplantation (LTx) is restricted by the development of chronic lung allograft dysfunction (CLAD). CLAD represents at least 2 sub-phenotypes: restrictive allograft syndrome (RAS) and bronchiolitis obliterans syndrome (BOS), of which the exact pathophysiology remain elusive. A previous study demonstrated that increased broncho-alveolar lavage eosinophilia predisposed to CLAD. We further investigated the presence of eosinophils in explants lung tissue of CLAD. MethodsSections of BOS (n=16) and RAS (n=16) lungs were stained and quantified compared to (non-transplant) control lungs (n=20). Eosinophils, identified by the marker EG2, were counted in three different compartments; around the airway, in the parenchyma and around the blood vessel. Results were represented as the mean number (±SEM) of cells per high power field. Sections of BOS (n=16) and RAS (n=16) lungs were stained and quantified compared to (non-transplant) control lungs (n=20). Eosinophils, identified by the marker EG2, were counted in three different compartments; around the airway, in the parenchyma and around the blood vessel. Results were represented as the mean number (±SEM) of cells per high power field. ResultsRepresentative staining of BOS (A), RAS (B) and control (C) are provided in figure 1. Around the airways, eosinophils were significantly increased in BOS (16.7±4.8; p<0.05) and in RAS (13.4±4.0; p<0.05) compared to control (2.8±0.8). In the parenchyma, there were more eosinophils present in BOS (8.8±1.4; p<0.05), but not in RAS (8.2±2.2), compared to control (3.9±0.9). Around the blood vessels, both BOS (11.4±2.1; p<0.01) and RAS (9.8±1.9; p<0.05) demonstrated an increased number of eosinophils compared to control (4.0±0.6). The number of eosinophils around the airways correlated with eosinophil numbers in the parenchyma (R=0.55, p<0.0001) and around the blood vessels (R=0.79, p<0.0001). Representative staining of BOS (A), RAS (B) and control (C) are provided in figure 1. Around the airways, eosinophils were significantly increased in BOS (16.7±4.8; p<0.05) and in RAS (13.4±4.0; p<0.05) compared to control (2.8±0.8). In the parenchyma, there were more eosinophils present in BOS (8.8±1.4; p<0.05), but not in RAS (8.2±2.2), compared to control (3.9±0.9). Around the blood vessels, both BOS (11.4±2.1; p<0.01) and RAS (9.8±1.9; p<0.05) demonstrated an increased number of eosinophils compared to control (4.0±0.6). The number of eosinophils around the airways correlated with eosinophil numbers in the parenchyma (R=0.55, p<0.0001) and around the blood vessels (R=0.79, p<0.0001). ConclusionEosinophils, regulated by a Th2 immune response, are increased in BOS and RAS which may implicate a new pathway. These findings may lead to additional therapeutic options to improve outcome after LTx in the future. Eosinophils, regulated by a Th2 immune response, are increased in BOS and RAS which may implicate a new pathway. These findings may lead to additional therapeutic options to improve outcome after LTx in the future." @default.
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• W2022338923 title "An Immunohistological Study To Evaluate the Role of Eosinophils in Chronic Lung Allograft Dysfunction" @default.
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