The retrovirus-induced murine AIDS (MAIDS) shares many features with human AIDS. Here, we examined the susceptibility of mice with MAIDS to staphylococcal enterotoxin-triggered shock. Following sensitization with D- galactosamine (D-Gal), mice with MAIDS were resistant to the otherwise lethal effect of superantigen staphylococcal enterotoxin A (SEA). Peak IL-2 levels in these mice after D-Gal/SEA challenge were 10-fold higher than those in uninfected controls, and concurrently, IL-10 levels rose markedly with reduction of circulating IL-1 and IFN-γ. Treatment with neutralizing anti- IL-10 mAb before D-Gal/SEA challenge led to increased IFN-γ levels in mice with MAIDS, and resulted in a dose-dependent mortality. In contrast, mice with MAIDS were more susceptible to the toxicity of bacterial endotoxin LPS than were uninfected controls. Administration of 100 mg LPS alone induced 50% lethality in mice infected with MAIDS virus 8 wk previously but not in uninfected controls. Administration of 10 μg LPS caused acute shock in D- Gal-sensitized mice with MAIDS. Peak TNF-α levels in these mice after LPS challenge were increased more than 10-fold, whereas IL-10 levels were one- third of those after SEA challenge. Moreover, serum IFN-γ was undetectabie in uninfected controls and rose to 1063 ± 483 pg/ml in mice with MAIDS 4 h after LPS challenge. These results suggest that aberrant profiles of cytokine production are crucial in determining fatal outcome in these two types of septic shock in MAIDS.
|Number of pages||7|
|Journal||Journal of Immunology|
|Publication status||Published - Jan 1 1995|
All Science Journal Classification (ASJC) codes