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

Jessica G. Moreland, Robert M. Fuhrman, Christine L. Wohlford-Lenane, Timothy J. Quinn, Erin Benda, Jonathan A. Pruessner, David A. Schwartz

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

To determine the role of tumor necrosis factor (TNF)-α and interleukin (IL)-1β in the lower respiratory tract inflammatory response after inhalation of lipopolysaccharide (LPS), we conducted inhalation exposure studies in mice lacking expression of TNF-α 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-α and IL-1β do not appear to have an essential role in mediating the physiological or inflammatory response to inhaled LPS.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number1 24-1
StatePublished - Jan 2001

Fingerprint

Interleukin-1
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Cytokines
Interleukin-1 Type I Receptors
Inhalation Exposure
Messenger RNA
Airway Resistance
Bronchoalveolar Lavage Fluid
Bronchoalveolar Lavage
Respiratory System
Inhalation
Pneumonia
Proteins
Lung
Population

Keywords

  • Airway inflammation
  • Asthma
  • Cytokines
  • Endotoxin
  • Interleukin-β
  • Lipopolysaccharide
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Cell Biology
  • Physiology
  • Physiology (medical)

Cite this

Moreland, J. G., Fuhrman, R. M., Wohlford-Lenane, C. L., Quinn, T. J., Benda, E., Pruessner, J. A., & Schwartz, D. A. (2001). TNF-α and IL-1β are not essential to the inflammatory response in LPS-induced airway disease. American Journal of Physiology - Lung Cellular and Molecular Physiology, 280(1 24-1).

TNF-α and IL-1β are not essential to the inflammatory response in LPS-induced airway disease. / Moreland, Jessica G.; Fuhrman, Robert M.; Wohlford-Lenane, Christine L.; Quinn, Timothy J.; Benda, Erin; Pruessner, Jonathan A.; Schwartz, David A.

In: American Journal of Physiology - Lung Cellular and Molecular Physiology, Vol. 280, No. 1 24-1, 01.2001.

Research output: Contribution to journalArticle

Moreland, JG, Fuhrman, RM, Wohlford-Lenane, CL, Quinn, TJ, Benda, E, Pruessner, JA & Schwartz, DA 2001, 'TNF-α and IL-1β are not essential to the inflammatory response in LPS-induced airway disease', American Journal of Physiology - Lung Cellular and Molecular Physiology, vol. 280, no. 1 24-1.
Moreland, Jessica G. ; Fuhrman, Robert M. ; Wohlford-Lenane, Christine L. ; Quinn, Timothy J. ; Benda, Erin ; Pruessner, Jonathan A. ; Schwartz, David A. / TNF-α and IL-1β are not essential to the inflammatory response in LPS-induced airway disease. In: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2001 ; Vol. 280, No. 1 24-1.
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