| Main Title |
Influenza Virus-Specific Cytotoxic T-Lymphocyte Activity in Fischer 344 Rat Lungs as a Method to Assess Pulmonary Immunocompetence: Effect of Phosgene Inhalation. |
| Author |
Ehrlich, J. P. ;
Gunnison, A. F. ;
Burleson., G. R. ;
|
| CORP Author |
Health Effects Research Lab., Research Triangle Park, NC. ;Northrop Services, Inc., Research Triangle Park, NC. ;New York Univ. Medical Center, NY. Inst. of Environmental Medicine. |
| Publisher |
c1989 |
| Year Published |
1989 |
| Report Number |
EPA/600/J-89/226; |
| Stock Number |
PB90-146044 |
| Additional Subjects |
Lungs ;
Respiration ;
Toxicity ;
Phosgene ;
Body weight ;
Rats ;
Exposure ;
Models ;
Infectious diseases ;
Reprints ;
T lymphocytes ;
Immunologic cytotoxicity ;
Orthomyxoviruses ;
Dose-response relationships
|
| Holdings |
| Library |
Call Number |
Additional Info |
Location |
Last
Modified |
Checkout
Status |
| NTIS |
PB90-146044 |
Some EPA libraries have a fiche copy filed under the call number shown. |
|
07/26/2022 |
|
| Collation |
12p |
| Abstract |
The study utilized a rat influenza virus-infectivity model to determine alterations in an important host antiviral immunological response following an acute 4.0 hr exposure to 1.0 ppm phosgene. The effect on the specific antiviral immune response of the pulmonary cytotoxic T lymphocyte (CTL) was determined as the measure of toxicity. A significant suppression in the CTL response was detected 10 days post infection, a time during which peak activity is normally detected in control rats. No alterations were detected in pulmonary cell populations at this time, indicating that phosgene exposure alters the functional CTL activity. The CTL activity is believed to be an important antiviral immunological defense mechanism. CTL activity is the first specific immunological defense mechanism; inadequate CTL activity resulting from toxicant exposure could result in an enhanced and significantly prolonged pulmonary virus infection. (Copyright (c) 1989 Hemisphere Publishing Corporation.) |
