Biomedical subjects
Publications and source records attributed to M A Chirigos.
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The in vitro effect of exogenously added prostaglandin (PG) E1 or E2 over concentrations ranges of from 1 X 10(-4) to 1 X 10(-9) M were studied in order to determine their effect on the in vitro lymphocyte proliferation of thymic and splenic T and B cells from normal and tumor-bearing CD2F1 mice. It was found that PGE1 generally caused greater inhibition of blastogenesis than did PGE2 when reacted with splenic lymphocytes from normal mice. Indeed, PGE2 was found to be stimulatory for both Con A- and LPS-sensitive normal splenic lymphocytes. Both PGE1 and PGE2 caused potent inhibition of Con A- and PHA-sensitive splenic lymphocytes from the tumor-bearing mice. Additionally, PGE2 was found to stimulate the LPS-reactive lymphocytes from the tumored mice. PGE1 and PGE2 both inhibited the Con A- and PHA-reactive thymic lymphocytes from normal mice at the lower concentrations studied, i.e., 10(-4) to 10(-6) M. Thereafter, at concentration ranges of from 10(-7) to 10(-9) M both PGE1 and PGE2 were both found to be stimulatory. Finally, both PGE1 and PGE2 at all concentrations studied, strongly inhibited the thymic lymphocytes from tumored mice.
The effect of pyran copolymer, injected into mice bearing the M109 Madison lung carcinoma, on serum concentrations of lysozyme, beta-glucuronidase, and N-acetyl-beta, D-glucosaminidase was studied and compared with that of other immunoadjuvants. Increases in lysozyme levels ranging from 50 to 100% were observed after injection of pyran, BCG and Bru-Pel; increases in the levels of the other enzymes were less consistent. Other immunoadjuvants were less effective in raising serum concentrations of lysosomal enzymes. The findings were correlated with the results of previous studies on macrophage activation and antineoplastic action produced by these immunoadjuvants and suggest that serum levels of lysozyme can serve as indices of these effects.
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The effect of exogenously added prostaglandin (PG) E1 or E2 over concentration ranges of from 1 x 10(-4) to 1 x 10(-9)M were studied in order to determine their effect on the delayed-type hypersensitivity (DtH) reaction of normal or tumored mice. PGE1 or PGE2 generally caused a stimulation over the control values of normal mice as detected by the footpad swelling assay. However, PGE1 or PGE2 at all concentrations tested were found to significantly inhibit the DtH reaction of CD2F1 tumored mice.
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The effects of i.p. and s.c. Adriamycin and cyclophosphamide treatment of BALB/c x DBA/2F1 mice were studied alone and in combination with immunotherapeutic agents, pyran copolymer and Bacillus Calmette-Guérin, on macrophage cytotoxic ability, As assessed by direct viable cell counts of MBL-2 leukemia cells, both Adriamycin and cyclophosphamide produced growth-inhibitory macrophages. This function after s.c. cytostatic treatment peaked at Day 1 and decreased progressively, attaining normal control values by Day 6. When adjuvants, such as pyran and B. Calmette-Guérin, were administered i.p. simultaneously with s.c. Adriamycin or cyclophosphamide, adjuvant-induced cytotoxic function was not markedly affected. A better knowledge of the influence of cytostatic agents alone or combined with immunoadjuvants on macrophage cytotoxic ability may be useful in designing more effective chemoimmunotherapy protocols.
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Alcohol appears to exert a depressive effect on host immunity. Animal models useful in studying immune responsiveness in cancer research are discussed, which could be of value in studying the effect of alcoholism. Allogeneic tumor grafts are poorly rejected in immunosuppressed mice. Of the four major cellular elements of the immune system, the macrophage appears to have a critical role in immune surveillance. Several conditions occur which abrogate or restrict the tumoricidal activity of macrophages. Stress induced by physical restraint results in depressed macrophage activation. The tumoricidal activation induced in macrophages by interferon was markedly depressed in the presence of the corticosteroids, hydrocortisone, prednisone, and dexamethasone. In addition, prostaglandins (PGE1 and PGE2) also were found to decrease interferon activation of macrophages. Since immune deficiency is a trait of alcoholism and cancer, animal models with defined, measurable, immunological parameters would be useful in studying the effect of alcohol on cellular immunity.
Exogenously added prostaglandins E1 and E2, but not F2alpha, inhibited the tumoricidal activity of interferon-activated macrophages of mice. A role for adenosine 3',5'-monophosphate (cyclic AMP) in modulating macrophage functional activity was suggested because prostaglandins of the E series increase intracellular concentrations of cyclic AMP in macrophages and because treatment of interferon-activated macrophages with dibutyryl cyclic AMP consistently inhibits expression of cytotoxicity. Since the activated macrophage releases high concentrations of prostaglandin E2, it is postulated that this prostaglandin could act locally in negative feedback inhibition to limit cell activities.
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With phenolphthalein beta-glucuronide as the substrate in the serum beta-glucuronidase assay, centrifugation at high speed after addition of alkali was required to minimize blanks. Optimal substrate concentration was 3--6 mM. Excess substrate was inhibitory.
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