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Am J Physiol Lung Cell Mol Physiol 280: L173-L180, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 1, L173-L180, January 2001

TNF-alpha and IL-1beta are not essential to the inflammatory response in LPS-induced airway disease

Jessica G. Moreland1, Robert M. Fuhrman1, Christine L. Wohlford-Lenane2, Timothy J. Quinn2, Erin Benda2, Jonathan A. Pruessner1, and David A. Schwartz2

1 Department of Pediatrics and 2 Pulmonary, Critical Care, and Occupational Medicine Division, Department of Internal Medicine, The University of Iowa, Iowa City, Iowa 52242

To determine the role of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta in the lower respiratory tract inflammatory response after inhalation of lipopolysaccharide (LPS), we conducted inhalation exposure studies in mice lacking expression of TNF-alpha and/or IL-1 receptor type 1 and in mice with functional blockade of these cytokines using adenoviral vector delivery of soluble receptors to one or both cytokines. Alterations in airway physiology were assessed by pulmonary function testing before and immediately after 4 h of LPS exposure, and the cellular inflammatory response was measured by whole lung lavage and assessment of inflammatory cytokine protein and mRNA expression. Airway resistance after LPS exposure was similarly increased in all groups of mice without evidence that blockade of either or both cytokines was protective from this response. Additionally, all groups of mice demonstrated significant increases in lung lavage fluid cellularity with a complete shift in the population of cells to a predominantly neutrophilic infiltrate as well as elevation in inflammatory cytokine protein and mRNA levels. There were no significant differences between the groups in measures of lung inflammation. These results indicate that TNF-alpha and IL-1beta do not appear to have an essential role in mediating the physiological or inflammatory response to inhaled LPS.

tumor necrosis factor-alpha ; interleukin-beta ; lipopolysaccharide; endotoxin; cytokines; asthma; airway inflammation


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