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. 1978 Jun;75(6):2893–2896. doi: 10.1073/pnas.75.6.2893

Bone marrow colony-stimulating factor and tumor resistance-enhancing activity of postendotoxin mouse sera

R Christopher Butler 1,*, Alexander M Abdelnoor 1,†, Alois Nowotny 1,‡
PMCID: PMC392671  PMID: 351621

Abstract

The passive transfer of postendotoxin mouse serum could enhance nonspecific resistance to the development of TA3-Ha transplantable ascites tumor in mice. The postendotoxin serum was not directly cytotoxic to TA3-Ha tumor cells in vitro, nor did it contain significant amounts of residual endotoxin, but it was rich in colony-stimulating factors (CSFs). High-titer CSF serum could be induced by endotoxic lipopolysaccharide (LPS). Nonendotoxic, lipid-free, and polysaccharide-rich hydrolytic breakdown product of LPS (called PS) was less potent but still active in CSF induction. There was a correlation between the level of CSF stimulation and the capacity of the sera to transfer tumor resistance (TUR). Those LPS preparations that had the highest CSF-inducing capacity were the most potent in TUR enhancement. Suppression of CSF production by treatment with theophylline or epinephrine, enhancers of cyclic AMP/cyclic GMP ratios, lowered the enhancement of TUR by endotoxic LPS. The infection of serum donor mice with bacillus Calmette-Guérin (BCG) 18 days prior to LPS treatment gave the highest serum CSF levels and the most potent TUR-inducing serum preparation. Even more notable was the finding that the nontoxic PS preparation could replace toxic LPS in the above BCG-LPS system. The serum harvested from BCG-infected mice 2 hr after PS injection was similarly effective in the passive transfer of TUR.

Keywords: TA3-Ha ascites tumor, passive transfer, lipopolysaccharide, tumor-necrotizing factor, anti-tumor resistance

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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