Compartmentalization of Intraalveolar and Systemic Lipopolysaccharide-Induced Tumor Necrosis Factor and the Pulmonary Inflammatory Response (original) (raw)
Journal Article
,
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Please address requests for reprints to Dr. Steve Nelson, Department of Pulmonary/Critical Care Medicine, Louisiana State University Medical Center, 1542 Tulane Avenue, New Orleans, Louisiana 70112.
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,
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Search for other works by this author on:
,
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Search for other works by this author on:
,
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Search for other works by this author on:
,
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Search for other works by this author on:
Departments of Pulmonary/Critical Care Medicine, Physiology, and Microbiology and Immunology, Louisiana State University Medical Center
,
New Orleans, Louisiana
Search for other works by this author on:
Revision received:
09 August 1988
Published:
01 February 1989
Cite
Steve Nelson, Gregory J. Bagby, Bruce G. Bainton, Lawrence A. Wilson, James J. Thompson, Warren R. Summer, Compartmentalization of Intraalveolar and Systemic Lipopolysaccharide-Induced Tumor Necrosis Factor and the Pulmonary Inflammatory Response, The Journal of Infectious Diseases, Volume 159, Issue 2, February 1989, Pages 189–194, https://doi.org/10.1093/infdis/159.2.189
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Abstract
Tumor necrosis factor-α (TNF), a mono kine produced by lipopolysaccharide (LPS)-stimulated macrophages, is an activator of phagocytic functions and may modulate host responses during infection. To determine the effects of LPS on TNF activity and the pulmonary inflammatory response in vivo, we challenged rats systemically or intratracheally with LPS. Intravenous LPS significantly increased serum TNF content from nondetectable levels in control specimens to peak levels at 90 min, which declined to baseline by 3 h. In response to intratracheal LPS, levels of TNF both in bronchoalveolar lavage fluid and associated with alveolar macrophages increased significantly from near nondetectable levels in control animals. Increases in TNF levels werec onfined to the LPS-challenged compartment. Intravenous LPS resulted in a decrease in the number of peripheral blood neutrophils and in sequestration of these cells within the pulmonary vasculature. In contrast, intratracheal LPS elicited a marked intraalveolar inflammatory response.
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© 1989 by The University of Chicago
Topic:
- tumor necrosis factors
- pulmonary vasculature
- lung
- immune response
- bronchoalveolar lavage fluid
- infectious mononucleosis
- lipopolysaccharides
- macrophages
- macrophages, alveolar
- neutrophils
- infections
- rats
- transcriptional activation
- tumor necrosis
- inflammatory response
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