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Divisions of 1 Medical Intensive Care and 2 Pulmonary Medicine, Department of Internal Medicine, University Hospital of Geneva, 1211 Geneva 14, Switzerland
Positive-pressure mechanical ventilation supports gas exchange
in patients with respiratory failure but is also responsible for
significant lung injury. In this study, we have developed an in vitro
model in which isolated lung cells can be submitted to a prolonged
cyclic pressure-stretching strain resembling that of conventional
mechanical ventilation. In this model, cells cultured on a Silastic
membrane were elongated up to 7% of their initial diameter,
corresponding to a 12% increase in cell surface. The lung macrophage
was identified as the main cellular source for critical inflammatory
mediators such as tumor necrosis factor-
, the chemokines interleukin
(IL)-8 and -6, and matrix metalloproteinase-9 in this model system of
mechanical ventilation. These mediators were measured in supernatants
from ventilated alveolar macrophages, monocyte-derived macrophages, and
promonocytic THP-1 cells. Nuclear factor-
B was found to be activated
in ventilated macrophages. Synergistic proinflammatory effects of
mechanical stress and molecules such as bacterial endotoxin were
observed, suggesting that mechanical ventilation might be particularly
deleterious in preinjured or infected lungs. Dexamethasone prevented
IL-8 and tumor necrosis factor- secretion in ventilated macrophages.
Mechanical ventilation induced low levels of IL-8 secretion by alveolar
type II-like cells. Other lung cell types such as endothelial cells,
bronchial cells, and fibroblasts failed to produce IL-8 in response to
a prolonged cyclic pressure-stretching load. This model is of
particular value for exploring physical stress-induced signaling
pathways, as well as for testing the effects of novel ventilatory
strategies or adjunctive substances aimed at modulating cell activation
induced by mechanical ventilation.
alveolar macrophages; tumor necrosis factor-; interleukin-8; interleukin-6; nuclear factor-B; metalloproteinases; ventilator-induced lung injury; acute respiratory distress syndrome
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