Steroids and tuftsin fail to prevent the induction of altered plasma proteinase homeostasis in mice bearing the B16 melanoma or treated with C. parvum.
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| Abstract |
The effects of tuftsin and steroids (methyl prednisolone) on the induction of disrupted plasma proteinase regulation in mice bearing the B16 melanoma or treated with Corynebacterium parvum was investigated. Tuftsin treatment inhibited tumor progression only if treatment was started at the time of tumor transplantation. However, tuftsin inhibited the development of splenomegaly in mice with established tumors. In contrast, tuftsin did not influence either the induction of elevated plasma proteinase activity or the activity in plasma from animals with established tumors. Treatment of mice with high, anti-inflammatory, doses of steroid (20 mg/kg/day) partially inhibited tumor progression, inhibited the induction of splenomegaly, but did not inhibit the induction of disrupted plasma proteinase regulation. Likewise, steroid treatment did not suppress the induction of elevated plasma proteinase activity following treatment of mice with C. parvum. Thus the induction of elevated plasma proteinase activity, previously demonstrated to be a host regulated phenomenon, is resistant to regulation by this anti-inflammatory drug and likely not a component of the anti-tumor response. These findings raise the possibility that this phenomenon results from the interaction of activated RES elements with components of the plasma proteinase cascades.
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| Authors | D A Hart |
| Journal | International journal of immunopharmacology (Int J Immunopharmacol) Vol. 9 Issue 6 Pg. 669-74 ( 1987) ISSN: 0192-0561 [Print] England |
| PMID | 3319918 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't) |
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