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Acute Lung Injury Induced by Staphylococcal enterotoxin B: Disruption of Terminal Vessels as a Mechanism of Induction of Vascular Leak

Published online by Cambridge University Press:  10 May 2012

Ali Imran Saeed ,
Sadiye Amcaoglu Rieder ,
Robert L. Price ,
James Barker ,
Prakash Nagarkatti  and
Mitzi Nagarkatti
Ali Imran Saeed
Affiliation:
Division of Pulmonology, Department of Internal Medicine, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Sadiye Amcaoglu Rieder
Affiliation:
Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Robert L. Price
Affiliation:
Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, SC 29209, USA
James Barker
Affiliation:
Division of Pulmonology, Department of Internal Medicine, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Prakash Nagarkatti
Affiliation:
Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29209, USA
Mitzi Nagarkatti*
Affiliation:
Department of Pathology, Microbiology and Immunology, University of South Carolina School of Medicine, Columbia, SC 29209, USA
*
Corresponding author. E-mail: [email protected]
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Abstract

The current hypothesis of alveolar capillary membrane dysfunction fails to completely explain the severe and persistent leak of protein-rich fluid into the pulmonary interstitium, seen in the exudative phase of acute lung injury (ALI). The presence of intact red blood cells in the pulmonary interstitium may suggest mechanical failure of pulmonary arterioles and venules. These studies involved the pathological and ultrastructural evaluation of the pulmonary vasculature in Staphylococcal enterotoxin B (SEB)-induced ALI. Administration of SEB resulted in a significant increase in the protein concentration of bronchoalveolar lavage fluid and vascular leak in SEB-exposed mice compared to vehicle-treated mice. In vivo imaging of mice demonstrated the pulmonary edema and leakage in the lungs of SEB-administered mice. The histopathological studies showed intense clustering of inflammatory cells around the alveolar capillaries with subtle changes in architecture. Electron microscopy studies further confirmed the diffuse damage and disruption in the muscularis layer of the terminal vessels. Cell death in the endothelial cells of the terminal vessels was confirmed with TUNEL staining. In this study, we demonstrated that in addition to failure of the alveolar capillary membrane, disruption of the pulmonary arterioles and venules may explain the persistent and severe interstitial and alveolar edema.

Keywords

electron microscopypulmonary vascular leakacute respiratory distress syndromeacute lung injury
Type
Biological Applications
Information
Microscopy and Microanalysis , Volume 18 , Issue 3 , June 2012 , pp. 445 - 452
Copyright
Copyright © Microscopy Society of America 2012

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