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Mechanical Ventilation of Various Human Lung Cells In Vitro*: Identification of the Macrophage as the Main Producer of Inflammatory Mediators

Irène Dunn; Jérôme Pugin, MD
Author and Funding Information

*From the Division of Medical Intensive Care, University Hospital of Geneva, Geneva, Switzerland. Supported by grants from the Swiss National Foundation for Scientific Research 32-40344.94 and 32-50764.97, the 3R Research Foundation, Switzerland, grant No. 46-96, the Lancardis, and the Prof. Dr. Max Cloëtta Foundations (J.P.), and by a biomedical and natural science research grant, Switzerland (I.D.).

Correspondence to Jérôme Pugin, MD, Division of Medical Intensive Care, Department of Medicine, University Hospital of Geneva, 1211 Geneva 14, Switzerland; e-mail: pugin@cmu.unige.ch



Chest. 1999;116(suppl_1):95S-97S. doi:10.1378/chest.116.suppl_1.95S
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Extract

Ventilator-induced lung injury (VILI) is the result of a complex interplay among various mechanical forces acting on alveoli during mechanical ventilation. Data from animal models strongly suggest that the two main determinants of VILI are alveolar overdistention and the repeated collapse and reopening of alveoli during the ventilatory cycle.12 Studies exploring the pathophysiologic mechanisms underlying VILI suggest that these forces probably exert their damaging effects through the initiation of a localized inflammatory response, the latter being responsible for ongoing lung injury.3 It is conceivable that injurious ventilatory regimens participate in lung injury and alveolar inflammation such as that observed during the ARDS. However, direct proinflammatory effects of the physical stress generated by positive pressure mechanical ventilation on lung cells have not been shown. In this work, we identify the lung macrophage as a critical mechanosensor cell capable of triggering lung inflammation in response to pressure/stretching mechanical forces.


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