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Biomedical subjects

H W Rogers

Publications and source records attributed to H W Rogers.

17 recordsLinked to original sources
PubMed1996

Listeria monocytogenes induces apoptosis of infected hepatocytes.

Infection with blood-borne Listeria monocytogenes results in their early uptake by the liver. Foci of hepatocytes become heavily infected and develop into microabscesses. Infection results in apoptosis of the hepatocytes. This is particularly evident in the edge of the microabscess, where hepatocytes are not yet destroyed by the neutrophil. It is also apparent when neutrophils are depleted from the circulation. Infection of hepatocytes in culture induces their death by apoptosis with the release of neutrophil chemoattractants. Cytokines do not reduce the multiplication of Listeria in cultured hepatocytes. This study calls attention to an early program of inflammation induced in infected cells that are unresponsive to cytokines.

Animals↗
PubMed1994

Comparison of spectrometric and autophotographic methods for determining DNA concentrations.

Earlier studies from this laboratory demonstrated that a lumigenic detection method could utilize liquid scintillation counters for quantitation of DNA. Advantages included: 1) elimination of the need for radioactive probes, 2) rapid localization of spots by exposure of X-ray film and 3) longer shelf life of probe DNA. A major disadvantage of cutting spots from the membrane for luminometric assay is the destruction (or consumption) of the membrane; another disadvantage is the length of time spent handling the membrane while trying to cut out individual spots. When transmittance was compared with counts per minute for target CAT DNA, both methods gave statistically significant differences between 10 and 100 picograms of target DNA but less than 10 picograms were not significantly distinguished by either method. The digitized x-ray films read by image analysis allowed reliable determination of target DNA concentrations and leaves the original membrane intact to serve as a permanent record of experiments.

Animals↗
PubMed1994

Endogenous IL-1 is required for neutrophil recruitment and macrophage activation during murine listeriosis.

By using a mixture of neutralizing mAbs to IL-1 alpha, IL-1 beta, and to the type I IL-1R, we previously documented a regulatory role for IL-1 in the development of anti-Listeria responses in mice. Both normal C.B-17 and severe combined immunodeficiency (SCID) mice injected with this mixture of Abs exhibit decreased resistance to Listeria. In this study, we demonstrate that the neutralization of IL-1 activity in SCID mice results in a major defect in neutrophil migration to the peritoneum, in response to Listeria infection. Moreover, anti-IL-1 treatment also inhibits Listeria-induced peripheral blood leukocytosis at all time points examined. We also show that mice injected with anti-IL-1 Abs failed to elaborate class II MHC-positive peritoneal macrophages in vivo at any time during Listeria infection. Even though peritoneal macrophages from anti-IL-1-treated Listeria-infected mice are not activated to express MHC class II molecules, IFN-gamma production in vivo is normal. Moreover, the macrophages are unresponsive to IFN-gamma in vitro, as assayed by MHC class II expression, even when rIL-1 is added. rIL-1 also is unable to increase the expression of IFN-gamma-induced surface class II MHC molecules on resident peritoneal macrophages in vitro. These results indicate that endogenously produced IL-1 plays an important role in Listeria-dependent neutrophil migration, increase in blood leukocyte number, generation of MHC class II-positive macrophages in vivo, and macrophage responsiveness to IFN-gamma.

Animals↗
PubMed1993

Release of nitric oxide during the T cell-independent pathway of macrophage activation. Its role in resistance to Listeria monocytogenes.

Immunodeficient mice are remarkably resistant to Listeria monocytogenes (LM) infection. We examined the role that nitric oxide (NO.) plays in the CB-17/lcr SCID (SCID) response to LM. SCID spleen cells produced large quantities of NO. (as measured by nitrite formation) when incubated in the presence of heat-killed LM. NO. production was dependent on the release of IFN-gamma by the SCID NK cells. When tested directly, macrophages produced large quantities of nitrite in response to LM, but only in the presence of IFN-gamma. The production of NO. induced by LM was not affected by neutralizing antibodies to TNF or IL-1. The production of NO. was inhibited by addition of either of two inhibitors of NO.synthase, NG-monomethyl arginine, or aminoguanidine. In a different situation, NK cells that were stimulated by TNF and Listeria products to release IFN-gamma did not produce NO.. Macrophages cultured with IFN-gamma killed live LM. This increased killing of LM was significantly inhibited by amino-guanidine. In vivo, administration of aminoguanidine resulted in a marked increase in the mortality and spleen bacterial loads of LM-infected SCID or immunocompetent control mice. We conclude that NO. is a critical effector molecule of T cell-independent natural resistance to LM as studied in the SCID mouse, and that the NO.-mediated response is essential for both SCID and immunocompetent host to survive after LM infection.

Amino Acid Oxidoreductases↗
PubMed1993

Neutrophils are involved in acute, nonspecific resistance to Listeria monocytogenes in mice.

The importance of neutrophils in killing extracellular, pyogenic bacteria has long been established. However, there is only indirect evidence for a role for neutrophils in resistance against intracellular organisms. In this study, we directly demonstrate the involvement of neutrophils in defense against Listeria monocytogenes in normal C.B-17 immunocompetent and C.B-17 SCID mice. Because of the lack of sterilizing T-cell immunity, SCID mice are unable to completely eliminate listeriae systemically and become chronically infected. Both immunocompetent and SCID mice treated with a specific neutrophil-depleting monoclonal antibody during the early stages of Listeria infection were rendered remarkably sensitive to the organism, with a high level of mortality resulting from enhanced bacterial growth. At a late stage of infection in SCID mice, however, administration of neutrophil-depleting antibody did not affect mortality. In spite of the neutrophil depletion, other parameters of nonspecific immune function were normal. Macrophage infiltration to the site of infection and macrophage expression of major histocompatibility complex class II molecules were unaffected. Moreover, NK cell functions were normal as measured by infiltration to an infection site and gamma interferon production. These data demonstrate an important role for neutrophils in controlling the acute phase of Listeria infection, cooperating with, and yet independent of, macrophages and NK cells.

Animals↗
PubMed1992

Interleukin 1 participates in the development of anti-Listeria responses in normal and SCID mice.

Using T- and B-cell deficient C.B-17 mice with the scid mutation, we have previously documented the existence of a T-cell-independent but interferon gamma-dependent pathway of macrophage activation that confers upon the host partial resistance to the facultative intracellular bacterium Listeria monocytogenes. This pathway is operative in both normal and SCID mice and consists of at least four components: interferon gamma, tumor necrosis factor, macrophages, and natural killer cells. Here we demonstrate that interleukin 1 also participates in this pathway but at a different site of action. Using monoclonal antibodies that neutralize the biologic activities of interleukin 1 alpha and interleukin 1 beta, we document that interleukin 1 participates neither directly in the induction of interferon gamma from isolated SCID natural killer cells nor in the antigen-specific activation of CD4+ T cells derived from Listeria-immune C.B-17 mice. In contrast, injection of a mixture of anti-interleukin 1 alpha, anti-interleukin 1 beta, and a newly derived monoclonal antibody specific for the murine type I interleukin-1 receptor into either SCID or normal C.B-17 mice blocked the in vivo elaboration of class II major histocompatibility complex-positive macrophages after infection of the animals with Listeria. Moreover, SCID mice treated with the anti-interleukin-1 mixture failed to control the growth of Listeria in vivo and eventually succumbed to the infection. These results document that endogenously produced interleukin 1 plays an obligate role in the Listeria-dependent induction of activated macrophages in vivo and demonstrate that the action of interleukin 1 is distinct from the generation of natural killer cell-derived interferon gamma.

Animals↗
PubMed1989

Interleukin 3-dependent and -independent mast cells stimulated with IgE and antigen express multiple cytokines.

In response to IgE and specific multivalent antigen, mast cell lines (both growth factor-dependent and -independent) induce the transcription and/or secretion of a number of cytokines having a wide spectrum of activities. We have identified IL-1, IL-3, IL-5, IL-6, IFN-gamma, GM-CSF, JE, MIP1 alpha, MIP1 beta, and TCA3 RNA in at least two of four mast cell clones. The production of these products (except JE) is activation-associated and can be induced by IgE plus antigen. In selected instances cytokine expression can also be induced by activation with Con A or phorbol ester plus ionophore, albeit to levels less than those observed with IgE plus antigen. In addition, long-term mast cell clones and primary cultures of bone marrow-derived mast cells specifically release IL-1, IL-4, and/or IL-6 bioactivity after activation. These findings suggest that in addition to their inflammatory effector function mast cells may serve as a source of growth and regulatory factors. The relationship of mast cells to cells of the T lymphocyte lineage is discussed.

Animals↗
PubMed1987

Determination of cell line suitability for rapid isolation of herpes simplex virus.

Herpes simplex virus (HSV) is one of the most commonly identified viruses in the clinical laboratory. HSV is of clinical consequence because of its ability to produce such life-threatening infections as encephalitis and neonatal disease. A variety of cell lines are currently being used for detection of HSV in cell culture. This study compared several cell lines simultaneously in a 96-well cell culture system to determine which lines demonstrated viral CPE most quickly following infection. In considering speed at which viral CPE is demonstrated, our results showed that primary rabbit kidney cells surpassed all other cell lines at 48 h post-viral infection. Alternative cell lines demonstrated to be suitable by this study were human fetal foreskin, human embryonic lung, and Vero cells.

Animals↗
PubMed1972

Protein kinase activity in equine herpesvirus.

A protein kinase which is intimately associated with equine herpesvirus (equine abortion virus) was found by using adenosine triphosphate-gamma-(32)P as a phosphate donor and virus protein as an acceptor. Consistent demonstration of the activity requires prior removal of phosphohydrolase. The kinase activity requires Mg(2+), is not stimulated by cyclic adenosine monophosphate, but is enhanced by added protamine or arginine-rich histone. The labeled product is resistant to ribonuclease, deoxyribonuclease, and chloroform-methanol but is sensitive to Pronase. Other tests suggest that serine and threonine residues are the acceptor sites. In the in vitro reaction, the incorporation represents an average of approximately 4,500 phosphate residues per virion, and all 17 virus protein bands resolved by polyacrylamide gel electrophoresis appear to be labeled.

Adenosine Triphosphate↗