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The Role of Alveolar Macrophage Beta-2 Adrenergic Receptors in Acute Lung Injury

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  • Title:
    The Role of Alveolar Macrophage Beta-2 Adrenergic Receptors in Acute Lung Injury
  • Author: Mutlu,Gokhan M
  • Subjects: albuterol ; ARDS(Acute Respiratory Distress Syndrome) ; ca2(carbonic anhydrase) ; CATECHOLAMINES ; EPINEPHRINE ; hk2(glycolysis) ; inflammation ; INFLUENZA ; LUNG ; MACROPHAGES ; Medicine and Medical Research ; metabolism ; pulmonary edema ; RNA SEQUENCE ANALYSIS ; VIRAL PNEUMONIA ; WOUNDS AND INJURIES
  • Description: The overall goal of this project is to understand how beta2AR signaling in macrophages contributes to Acute Respiratory Distress Syndrome, which is a significant contributor to morbidity and mortality in military and civilian settings. To achieve this goal, we proposed three specific aims. In Aim 1, we proposed to determine whether beta2-agonists worsen influenza A-induced lung injury via beta2ARs on tissue-resident and/or monocyte-derived alveolar macrophages. In Aim 2, we aimed to investigate whether IL-6 and/or recruitment of monocyte derived macrophages are required for the effects of 2ARs activation on influenza A-induced lung injury. In Aim 3, we proposed to determine whether inhibition of beta2ARs attenuates age-related worsening of influenza A-induced acute lung injury. In this reporting period, we confirmed that beta2ARs on monocytes and macrophages are critical for influenza A virus-induced acute lung injury. We developed and validated a method to clearly identify tissue resident and monocyte-derived macrophages. Our findings suggest that recruited monocyte derived, but not resident macrophages are responsible for the influenza-induced acute lung injury. We also discovered that beta2AR signaling in macrophages may regulate influenza-induced metabolic changes, which are required for pro-inflammatory response against influenza suggested by attenuation of inflammation with inhibitors of glycolysis (Hk2) and carbonic anhydrase (Ca2).
  • Creation Date: 2017
  • Language: English
  • Source: DTIC STINET
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