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Biomedical subjects

S W Russell

Publications and source records attributed to S W Russell.

At least 73 records · Page 4Linked to original sources
PubMed1982

Mitogenic activity elaborated by macrophage-like cell lines acts as competence factor(s) for BALB/c 3T3 cells.

The culture medium from several murine macrophage-like cell lines contained a mitogenic activity that functioned synergistically with platelet-poor plasma to induce DNA synthesis in quiescent density-inhibited BALB/c 3T3 fibroblasts. This mitogenic activity was generated by P388D1 (and other established lines of) macrophage-like cells that were cultured either in medium alone or in medium supplemented with platelet-poor plasma. The amount of mitogenic activity produced was directly related to the length of time the macrophage-like cells were maintained in the medium. Serum-free medium conditioned by macrophage-cells did not stimulate DNA synthesis in density-inhibited 3T3 cells in the absence of plasma; however, a transient (4-hr) exposure to serum-free macrophage-conditioned medium allowed quiescent cells to respond to plasma-derived progression factors. The addition of plasma to 3T3 cells that had been treated with the macrophage-conditioned medium brought about DNA synthesis after a 12-hr lag. The mitogenic activity that was in macrophage-conditioned medium bound to DEAE-Sephadex and eluted in a single peak using a linear NaCl gradient. This macrophage-derived competence factor was not mitogenic for lymphocytes and was clearly separated by DEAE-Sephadex chromatography from the major peak of the previously described mitogenic monokine, Interleukin-1 (lymphocyte activating factor).

Animals↗
PubMed1982

Regulation of macrophage-mediated tumor cell killing by prostaglandins: comparison of the effects of PGE2 and PGI2.

Mouse resident peritoneal macrophages stimulated in vitro by purified bacterial lipopolysaccharide (LPS) produced both prostaglandin E2 (PGE2) and prostaglandin I2 (PGI2), the latter detected as its stable metabolite, 6-keto PGF1 alpha. Maximum production, induced in each case by 1 ng/ml purified LPS, was in the range of 10(-7)M for PGI2 and 3 x 10(-8)M for PGE2. A quantitatively similar increase in intracellular levels of macrophage cyclic AMP (measured on a whole cell basis), with a similar duration of effect, was stimulated by PGE2 and PGI2; however, only PGE2 had a negative regulatory effect on macrophage activation for tumor cell killing. These data confirm that more than a whole cell increase in the concentration of cyclic AMP is needed to shut off nonspecific tumor cell killing mediated by LPS-activated resident peritoneal macrophages.

Animals↗
PubMed1982

Mouse mononuclear phagocyte antigenic heterogeneity detected by monoclonal antibodies.

Identification and characterization of the many cellular and subcellular changes that underlie various macrophage functions have been hampered by the problem of population heterogeneity. The problem has remained because, in the case of most functions, we have not had the means to examine cells at a level below that of whole populations. We report here the potential means to do so. Rat anti-mouse mononuclear phagocyte monoclonal antibodies were raised against adherent cells cultured from bone marrow. These antibodies were used to delineate and, in the presence of complement, eliminate subpopulations of macrophages. The extent to which antigenic heterogeneity occurs was shown in several mononuclear phagocyte populations that are commonly employed experimentally. Some antibodies reacted with most mononuclear phagocytes tested, whereas others showed marked selectivity of binding. As expected, resident populations were less heterogeneous antigenically than inflammatory populations were. The data both extend what is known about mononuclear phagocyte population heterogeneity and suggest means by way of which this heterogeneity can be overcome.

Animals↗
PubMed1981

Yersinia pseudotuberculosis infection: study of an epizootic in squirrel monkeys.

An epizootic of an acutely fatal enteric disease in a colony of squirrel monkeys (Saimiri sciureus) was attributed to infection by Yersinia pseudotuberculosis serotype III. Of a total adult population of 96 animals at risk, there were six fatal cases of yersiniosis. Serological evaluation of the colony just after the outbreak ended revealed that 22 of 60 monkeys tested (37%) had significant antibody to Y. pseudotuberculosis (microagglutination titer of greater than or equal to 1:80) but did not have clinical disease. The outstanding pathological lesions noted in dying monkeys were acute, purulent, necrotic and focal enteritis primarily affecting the jejunum and ileum and focal hepatic necrosis and abscessation. Y. pseudotuberculosis was isolated from the organs of two of the dying monkeys. Using cold enrichment techniques, Yersinia was also isolated from the feces of two apparently healthy monkeys (both seropositive), from the spleen of a monkey dying of other causes, and from the colon contents of a stillborn squirrel monkey baby. All isolates had the same biotype and serotype. An episode of abortions was associated both temporally and spatially with the fatal cases of yersiniosis, and Y. pseudotuberculosis was cultured from the uterus of two of the dying monkeys, suggesting that yersinia infection may be associated with abortion, as well as with enteric infection, in these animals.

Abortion, Veterinary↗
PubMed1981

Lymphokine maintains macrophage activation for tumor cell killing by interfering with the negative regulatory effect of prostaglandin E2.

Mouse resident peritoneal macrophages activated with bacterial lipopolysaccharide (LPS) rapidly lost their ability to kill tumor cells in vitro. Such loss of killing has previously been attributed to the effects of prostaglandin E (PGE) produced by the LPS-stimulated macrophages. Macrophages exposed in the current study to both LPS and partially purified lymphokine did not lose cytolytic activity, in spite of the fact that these cells produced undiminished amounts of PGE, compared to controls. Cytolytic activity was shown to be retained under these conditions because lymphokine decreased the sensitivity of activated macrophages to the negative regulatory effects of PGE. The mechanism responsible for the lymphokine effect is not known; however, generalized inhibition of macrophage responsiveness to the hormone does not appear to be involved because lymphokine did not reduce the cyclic AMP response of macrophages, measured on a whole cell basis, after they were exposed to PGE.

Animals↗
PubMed1981

Activation of mouse macrophages for tumor cell killing. I. Quantitative analysis of interactions between lymphokine and lipopolysaccharide.

Lymphokine-rich supernatants from concanavalin A-stimulated spleen cell cultures failed to activate mouse peritoneal macrophages for tumor cell killing, providing that the assay system was free of detectable (less than 0.125 ng/ml) endotoxin. Instead, increasing amounts of lymphokine progressively increased the sensitivity of macrophages to activation by purified bacterial lipopolysaccharide (LPS). Conversely, the effect of minute amounts of lymphokine could be detected in the presence of relatively high (though nonactivating) concentrations of LPS. The latter observation was exploited to develop a highly sensitive, quantitative assay for lymphokine. In this assay, serially diluted supernatants were tested on macrophage monolayers in the presence of a constant concentration (3 ng/ml) of LPS. Under these conditions, the lymphokine dose-response curve was sigmoidal and therefore suitable for conversion to a linear plot using the logarithmic transformation of the von Krogh equation. Activity could be expressed quantitatively and reproducibly in terms of units of activity. By facilitating purification the assay should contribute to the development of a more precise biochemical understanding of the role of lymphokine in macrophage activation for tumor cell killing.

Animals↗
PubMed1981

Macrophage-mediated tumor cell killing: regulation of expression of cytolytic activity by prostaglandin E.

The expression of nonspecific macrophage-mediated tumoricidal activity in vitro is a transient phenomenon. The work reported here shows that the loss of tumoricidal activity by mouse macrophages is attributable, at least in part, to the effects of prostaglandin E (PGE). The amount of PGE needed to inhibit the expression of cytolytic activity (2 x 10(-9) M) was readily synthesized and secreted by the same population of resident peritoneal macrophages that had been induced to kill tumor cells by exposure to 100 ng/ml bacterial lipopolysaccharide (LPS). Inhibitory concentrations of PGE were present in supernatants within the 1st hr after macrophages were exposed to LPS. In spite of this fact, cytolytic activity still developed, and 12 to 16 hr were required for the PGE to have its full inhibitory effect. Thus, PGE did not act by blocking the development of cytolytic activity. Treatment of LPS-stimulated macrophages with 10(-6) M indomethacin (or other cyclooxygenase inhibitors) prevented both PGE synthesis and the shut-off of cytolytic activity. The latter effect could be reversed by adding PGE2 to the cultures at a concentration of 10(-8) M. Lastly, PGE inhibited cytolytic activity mediated by indomethacin-treated macrophages only when activator was present: pulsing with PGE before the addition of LPS had a negligible inhibitory effect. These findings may help explain why intratumoral macrophages often lack nonspecific cytolytic capabilities.

Animals↗
PubMed1980

A discrete population of mononuclear phagocytes detected by monoclonal antibody.

Rat monoclonal antibody raised against cultured mouse bone marrow was used to detect an antigenic determinant on a discrete population of mouse mononuclear phagocytes by indirect immunofluorescence. The antigen was expressed on adherent, late-cultured bone marrow macrophages and chronic inflammatory peritoneal macrophages elicited by the injection of thioglycolate broth. Binding of the antibody to resident peritoneal or alveolar macrophages, blood monocytes, or freshly explanted bone marrow cells was not detected. Less than 10% of acute inflammatory mononuclear phagocytes expressed the antigen. The antibody did not bind detectably to lymphocytes, granulocytes, erythrocytes, fibroblasts, or the cells of several murine tumor lines. Results suggesting binding to mast cells were equivocal. The antigen was species, but not strain, specific. It was concluded that maturation, at least, was required for expression of the antigen. Results suggested that additional influences were also involved.

Animals↗