common.study.topics.clinical

Alveolar Macrophage Programming Following Endotoxin Exposure

common.study.values.description

Alveolar Macrophage Programming Following Endotoxin Exposure

The histologic hallmarks of lung inflammation include accumulation of inflammatory cells in the airspaces and interstitium, injury to alveolar epithelial and endothelial cells, loss of epithelial-capillary integrity and accumulation of edema fluid in the interstitium and airspaces. Accordingly, for alveolar repair to occur inflammation must be halted, debris and inflammatory cells removed, injured tissue cells replaced, and capillary barrier function re-established. Macrophages are key players in all of these. Here the investigators hypothesize that resident alveolar macrophages and recruited macrophages serve completely different functions, acting independently (i.e. division of labor) yet cooperatively (synergism).

common.study.values.location

participant.ui.study.affiliations-map.online-study.header-virtual

participant.ui.study.affiliations-map.online-study.text

participant.ui.study.affiliations-map.legend.locations participant.ui.study.affiliations-map.legend.selected

common.study.values.methods

No pharmaceutical medication involved common.study.methods.has-drugs-no
Patients and healthy individuals accepted common.study.methods.is-healthy-no

bronchoscopy with intrabronchial administration of lipopolysaccharide

The PI will administer intrabronchial LPS into the lungs of healthy volunteers and then obtaining macrophages by bronchoalveolar lavage (BAL) 24, 48, 72, 96, or 120 hours later.

participant.views.study.view.additional

participant.views.study.view.scientific-title

Alveolar Macrophage Programming Following Endotoxin Exposure

common.study.values.clinical-trial-id

NCT03859050

participant.views.study.view.id

eXDX8e