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Cachectin/tumor necrosis factor production by fetal and newborn rat hepatic macrophages
M L Silen1, D G Hesse, D Felsen
1Laboratories of Surgical Metabolism, New York Hospital, New York City.
Abstract:
The capacity of fetal and newborn hepatic macrophages to produce cachectin/tumor necrosis factor (TNF) has not been previously examined. The role that TNF plays in newborn infection is also unknown. In the present report, fetal and newborn rat hepatic macrophages have been maintained in short-term tissue culture, and are shown to produce TNF in response to in-vitro endotoxin stimulation. Cells obtained are morphologically and antigenically consistent with macrophages, and are depleted of accessory cells and lymphocytes. In response to increasing doses of endotoxin, fetal and newborn hepatic macrophages produce TNF, and this production is suppressed fully by pretreatment with dexamethasone. The results demonstrate that fetal and newborn hepatic macrophages possess the capability to produce TNF in vitro. We propose that TNF may play a role in the response of the fetus and newborn to bacterial infection.
Insights
Fetal and newborn rat liver macrophages can produce tumor necrosis factor (TNF) when stimulated with endotoxin. This finding suggests TNF may be important in fighting bacterial infections in newborns.
Area of Science:
- Immunology
- Neonatal Biology
- Cellular Biology
Background:
- The production of cachectin/tumor necrosis factor (TNF) by fetal and newborn hepatic macrophages is not well understood.
- The specific role of TNF in neonatal infections remains largely unknown.
Purpose of the Study:
- To investigate the capacity of fetal and newborn rat hepatic macrophages to produce TNF.
- To explore the potential role of TNF in neonatal immune responses to bacterial infection.
Main Methods:
- Fetal and newborn rat hepatic macrophages were cultured in vitro.
- Macrophages were stimulated with varying doses of endotoxin.
- TNF production was measured, and the effect of dexamethasone pretreatment was assessed.
- Cellular identity was confirmed morphologically and antigenically, with depletion of accessory cells and lymphocytes.
Main Results:
- Fetal and newborn hepatic macrophages demonstrated the ability to produce TNF in response to in vitro endotoxin stimulation.
- TNF production increased with higher endotoxin doses.
- Dexamethasone pretreatment completely suppressed TNF production.
- The cultured cells were confirmed to be macrophages, free of significant contamination by other cell types.
Conclusions:
- Fetal and newborn hepatic macrophages are capable of producing TNF in vitro.
- TNF may play a significant role in the immune response of the fetus and newborn to bacterial infections.