Studies on the endotoxin induced tumor resistance.
In summary, this report has discussed the immunologic mechanisms involved in the enhancement of nonspecific resistance to tumor by endotoxin. The optimal conditions for tumor protection involved pretreatment with approximately 25 mug LPS administered at the siteof subsequent tumor challenge. In an attempt to relate endotoxin structural components to the ability to enhance TUR, a variety of whole LPS's, endotoxic glycolipids and PS preparations were compared. While all of the intact LPS's and several of the glycolipids were effective in enhancing TUR, some endotoxic glycolipids were totally inactive although they were equally toxic. Some lipid-free PS preparations were also active although less than whole LPS. Evidence was presented to suggest that mechanism for enhancement of TUR involves B cells and macrophages but not T cells. The mechanism also involves the production of soluble factors which are released into the serum of mice in response to LPS or PS. These factors can transfer and mediate the antitumor effects of LPS. The preinfection of mice with BCG enhanced the activity of LPS and PS in the production of antitumor activity.
D000818:Animals; D002286:Carcinoma, Ehrlich Tumor / Q000401:mortality / Q000517:prevention & control*; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli / Q000276:immunology; D005260:Female; D007116:Immunization, Passive; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008805:Mice, Inbred A; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008813:Mice, Inbred ICR; D008819:Mice, Nude; D012475:Salmonella / Q000276:immunology; D012486:Salmonella typhimurium / Q000276:immunology; D012706:Serratia marcescens / Q000276:immunology
D004731:Endotoxins; D008070:Lipopolysaccharides