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Am J Physiol Lung Cell Mol Physiol (November 7, 2008). doi:10.1152/ajplung.00467.2007
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Submitted on November 9, 2007
Accepted on October 24, 2008

Mechanical ventilation enhances lung inflammation and caspase activity in a model of mouse pneumovirus infection

Reinout Alexander Bem1, Job B. M. van Woensel1, Albert P Bos1, Amy Koski2, Alex W Farnand3, Joseph B. Domachowske4, Helene F. Rosenberg5, Thomas R. Martin2, and Gustavo Matute-Bello3*

1 Pediatric Intensive Care Unit, Emma Children's Hospital/Academic Medical Center, Amsterdam, Netherlands
2 Department of Medicine, University of Washington School of Medicine, VA Puget Sound Health Care System and Division of Pulmonary and Critical Care Medicine, Seattle, Washington, United States
3 Department of Medicine, University of Washington School of Medicine, Center for Lung Biology, Division of Pulmonary and Critical Care Medicine, Seattle, Washington, United States
4 Pediatrics, SUNY Upstate Medical University, Syracuse, New York, United States
5 Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States

* To whom correspondence should be addressed. E-mail: matuteb{at}u.washington.edu.

Severe infection with respiratory syncytial virus (RSV) in children can progress to respiratory distress and acute lung injury (ALI). Accumulating evidence suggests that mechanical ventilation (MV) is an important cofactor in the development of ALI by modulating the host immune responses to bacteria. This study investigates whether MV enhances the host response to pneumonia virus of mice (PVM), a mouse pneumovirus that has been used as a model for RSV infection in humans. BALB/c mice were inoculated intranasally with diluted clarified lung homogenates from mice infected with PVM strain J3666 or uninfected controls. Four days after inoculation the mice were subjected to 4 hr of MV (Vt 10 ml/kg), or allowed to breathe spontaneously. As compared with mice inoculated with PVM-only, the administration of MV to PVM-infected mice resulted in increased bronchoalveolar lavage fluid (BALF) concentrations of the cytokines MIP-2, MIP-1{alpha} (CCL3) and IL-6; increased alveolar-capillary permeability to high molecular weight proteins; and increased caspase-3 activity in lung homogenates. We conclude that MV enhances the activation of inflammatory and caspase cell death pathways in response to pneumovirus infection. We speculate that MV potentially contributes to the development of lung injury in patients with RSV infection.




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