| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Division of Pulmonary, Allergy & Critical Care, Center for Translational Research of the Lung Mckelvey Center for Lung Transplantation, Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA
* To whom correspondence should be addressed. E-mail: mrojas{at}emory.edu.
Acute Lung Injury (ALI) is usually a complication of sepsis and endotoxin treatment of mice is a frequently used experimental model. To define this model and to clarify pathogenesis of the lung injury, we injected with 1 mg/kg endotoxin i.p. and measured pulmonary function, pulmonary edema, serum concentrations of cytokines and growth factors, and lung histology over 48h. During the first 6h tidal volume and minute volume increased, respiratory frequency decreased. Serum concentrations of cytokines showed 3 patterns: ten cytokines peaked at 2h and declined rapidly; two peaked at 6h and declined; and two had a biphasic peaks at 2h and 24h. Growth factors increased later and remained elevated longer. Both collagen and fibronectin were deposited in the lungs beginning within hours of endotoxin and resolving over 48h. Histologically, lungs showed increased cellularity at 6h with minimal persistent inflammation at 48h. Lung water peaked at 6h and gradually decreased over 48h. We conclude that intraperitoneal administration of endotoxin to mice causes a transient systemic inflammatory response and transient lung injury and dysfunction. The response is characterized by successive waves of cytokine release into the circulation, early evidence of lung fibrogenesis and prolonged increases in growth factors that may participate in lung repair.
This article has been cited by other articles:
|
|
 |
|
  J. Xu, C. R. Woods, A. L. Mora, R. Joodi, K. L. Brigham, S. Iyer, and M. Rojas Prevention of endotoxin-induced systemic response by bone marrow-derived mesenchymal stem cells in mice Am J Physiol Lung Cell Mol Physiol, July 1, 2007; 293(1): L131 - L141. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. B. Allen, T. Leclair, M. Cloutier, J. Thompson-Figueroa, and J. H. T. Bates The response to recruitment worsens with progression of lung injury and fibrin accumulation in a mouse model of acid aspiration Am J Physiol Lung Cell Mol Physiol, June 1, 2007; 292(6): L1580 - L1589. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. A. Jacob, K. M. Porter, S. C. Elms, P.-Y. Cheng, D. P. Jones, and R. L. Sutliff HIV-1-induced pulmonary oxidative and nitrosative stress: exacerbated response to endotoxin administration in HIV-1 transgenic mouse model Am J Physiol Lung Cell Mol Physiol, October 1, 2006; 291(4): L811 - L819. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. B. Santos, L. K. S. Nagato, N. M. Boechem, E. M. Negri, A. Guimaraes, V. L. Capelozzi, D. S. Faffe, W. A. Zin, and P. R. M. Rocco Time course of lung parenchyma remodeling in pulmonary and extrapulmonary acute lung injury J Appl Physiol, January 1, 2006; 100(1): 98 - 106. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Kubo Is Cell Therapy in Acute Lung Injury a Realistic Dream? Am. J. Respir. Crit. Care Med., October 1, 2005; 172(7): 794 - 795. [Full Text] [PDF]
|
|
|
|
|
|
Z. Zhou, J. Kozlowski, and D. P. Schuster Physiologic, Biochemical, and Imaging Characterization of Acute Lung Injury in Mice Am. J. Respir. Crit. Care Med., August 1, 2005; 172(3): 344 - 351. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
