The role of cytokines during the pathogenesis of ventilator-associated and ventilator-induced lung injury.
Mortality rates from acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) range from 30 to 65%. Although mechanical ventilation (MV) may delay mortality in critically ill patients with ALI/ARDS, it may also cause a lung injury that further promotes and perpetuates ALI/ARDS and multiorgan dysfunction syndrome (MODS). Recent studies have demonstrated that lung protective strategies of MV, as compared with the injurious strategy of conventional MV (CMV) can reduce absolute mortality rates during ALI/ARDS. The protective strategies limit tidal volumes and peak/plateau pressures while maximizing positive end-expiratory pressure. The injury to the lung by CMV is characterized histologically by edema, leukocyte extravasation, and endothelial and epithelial damage. Both human and animal studies suggest that alveolar cell deformation from CMV leads to the release of cytokines/chemokines which orchestrate the extravasation, activation, and recruitment of leukocytes, causing ventilator-associated lung injury (VALI) and ventilator-induced lung injury (VILI). Moreover, VALI/VILI can perpetuate the chronic inflammatory response during ALI/ARDS and MODS. This article explores the role of cytokines/chemokines during the pathogenesis of VALI/VILI.
Belperio
John A
JA
Department of Medicine, Division of Pulmonary and Critical Care Medicine at The David Geffen School of Medicine at UCLA, Los Angeles, California 90095, USA. jbelperio@mednet.ucla.edu
Keane
Michael P
MP
Lynch
Joseph P
JP
Strieter
Robert M
RM
D000818:Animals; D016207:Cytokines / Q000378:metabolism*; D006801:Humans; D012128:Respiratory Distress Syndrome / Q000209:etiology* / Q000378:metabolism / Q000628:therapy; D048069:Tumor Necrosis Factors / Q000378:metabolism; D012122:Ventilators, Mechanical / Q000009:adverse effects*
D016207:Cytokines; D048069:Tumor Necrosis Factors