Inflammatory Cellular Response to Mechanical Ventilation in Elastase-Induced Experimental Emphysema: Role of Preexisting Alveolar Macrophages Infiltration
المؤلفون المشاركون
Rouze, Anahita
Voiriot, Guillaume
Guivarch, Elise
Roux, Françoise
Tran Van Nhieu, Jeanne
Isabey, Daniel
Brochard, Laurent
Maitre, Bernard
Mekontso-Dessap, Armand
Boczkowski, Jorge
المصدر
العدد
المجلد 2018، العدد 2018 (31 ديسمبر/كانون الأول 2018)، ص ص. 1-10، 10ص.
الناشر
Hindawi Publishing Corporation
تاريخ النشر
2018-12-19
دولة النشر
مصر
عدد الصفحات
10
التخصصات الرئيسية
الملخص EN
An excessive pulmonary inflammatory response could explain the poor prognosis of chronic obstructive pulmonary disease (COPD) patients submitted to invasive mechanical ventilation.
The aim of this study was to evaluate the response to normal tidal volume mechanical ventilation in an elastase-induced murine model of pulmonary emphysema.
In this model, two time points, associated with different levels of lung inflammation but similar lung destruction, were analyzed.
C57BL/6 mice received a tracheal instillation of 5 IU of porcine pancreatic elastase (Elastase mice) or the same volume of saline (Saline mice).
Fourteen (D14) and 21 (D21) days after instillation, mice were anesthetized, intubated, and either mechanically ventilated (MV) or maintained on spontaneous ventilation (SV) during two hours.
As compared with Saline mice, Elastase mice showed a similarly increased mean chord length and pulmonary compliance at D14 and D21, while bronchoalveolar lavage cellularity was comparable between groups.
Lung mechanics was similarly altered during mechanical ventilation in Elastase and Saline mice.
Activated alveolar macrophages CD11bmid were present in lung parenchyma in both Elastase SV mice and Elastase MV mice at D14 but were absent at D21 and in Saline mice, indicating an inflammatory state with elastase at D14 only.
At D14, Elastase MV mice showed a significant increase in percentage of neutrophils in total lung, as compared with Elastase SV mice.
Furthermore, alveolar macrophages of Elastase MV mice at D14 overexpressed Gr1, and monocytes showed a trend to overexpression of CD62L, compared with Elastase SV mice.
In an elastase-induced model of pulmonary emphysema, normal tidal volume mechanical ventilation may produce an increase in the proportion of pulmonary neutrophils, and an activation of alveolar macrophages and pulmonary monocytes.
This response seems to be observed only when the emphysema model shows an underlying inflammation (D14), reflected by the presence of activated alveolar macrophages CD11bmid.
نمط استشهاد جمعية علماء النفس الأمريكية (APA)
Rouze, Anahita& Voiriot, Guillaume& Guivarch, Elise& Roux, Françoise& Tran Van Nhieu, Jeanne& Isabey, Daniel…[et al.]. 2018. Inflammatory Cellular Response to Mechanical Ventilation in Elastase-Induced Experimental Emphysema: Role of Preexisting Alveolar Macrophages Infiltration. BioMed Research International،Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1127470
نمط استشهاد الجمعية الأمريكية للغات الحديثة (MLA)
Rouze, Anahita…[et al.]. Inflammatory Cellular Response to Mechanical Ventilation in Elastase-Induced Experimental Emphysema: Role of Preexisting Alveolar Macrophages Infiltration. BioMed Research International No. 2018 (2018), pp.1-10.
https://search.emarefa.net/detail/BIM-1127470
نمط استشهاد الجمعية الطبية الأمريكية (AMA)
Rouze, Anahita& Voiriot, Guillaume& Guivarch, Elise& Roux, Françoise& Tran Van Nhieu, Jeanne& Isabey, Daniel…[et al.]. Inflammatory Cellular Response to Mechanical Ventilation in Elastase-Induced Experimental Emphysema: Role of Preexisting Alveolar Macrophages Infiltration. BioMed Research International. 2018. Vol. 2018, no. 2018, pp.1-10.
https://search.emarefa.net/detail/BIM-1127470
نوع البيانات
مقالات
لغة النص
الإنجليزية
الملاحظات
Includes bibliographical references
رقم السجل
BIM-1127470
قاعدة معامل التأثير والاستشهادات المرجعية العربي "ارسيف Arcif"
أضخم قاعدة بيانات عربية للاستشهادات المرجعية للمجلات العلمية المحكمة الصادرة في العالم العربي
تقوم هذه الخدمة بالتحقق من التشابه أو الانتحال في الأبحاث والمقالات العلمية والأطروحات الجامعية والكتب والأبحاث باللغة العربية، وتحديد درجة التشابه أو أصالة الأعمال البحثية وحماية ملكيتها الفكرية. تعرف اكثر