Cellular and Molecular Changes of the Respiratory System in Rats Exposed to ACM Combustion
Abstract
Rats exposed to advanced composite materials (ACM) combustion atmospheres develop a time dependent pulmonary inflammation characterized by the influx of polymorphonuclear neutrophils (PMNs) into the lumen of the lung, epithelial permeability changes and inflammatory cytokine release. Mice with defective tumor necrosis factor alpha (TNF-alpha) gene produced significantly less interleukin-l beta (IL-1beta) and IL-6 while mice with defective IL-1beta gene produced significantly more TNF-alpha with on effect on IL-6. Both strains had significantly fewer BALF cells and PMNs but no effect on epithelial permeability. The use of antibodies towards TNF-alpha and IL-1beta had no effect on epithelial permeability, BALF IL-1beta or TNF-alpha. IL-1beta antibodies did not affect BALF cell numbers but did significantly increase PMNs. No effect was noted on IL-6 levels with anti-IL-1beta. TNF-alpha antibodies significantly increased the BAbF cell numbers and IL-6 but significantly decreased the percentage of PMNs in the BALF. In conclusion, gene silencing was effective in reducing the inflammation (TNF-alpha > IL-1beta) from ACM combustion atmospheres while pretreatment with TNF-alpha or IL-1beta antibodies under the current protocol is ineffective.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 2003
- Accession Number
- ADA422009
Entities
People
- Paul G. Reinhart
Organizations
- Naval Health Research Center