The Experts below are selected from a list of 7926 Experts worldwide ranked by ideXlab platform
R. Van Furth - One of the best experts on this subject based on the ideXlab platform.
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Endogenous tumor necrosis factor alpha is required for enhanced antimicrobial activity against Toxoplasma gondii and Listeria monocytogenes in Recombinant Gamma Interferon-treated mice.
Infection and immunity, 1992Co-Authors: J. A. M. Langermans, M. E. B. Van Der Hulst, P. H. Nibbering, R. Van FurthAbstract:In vitro studies have shown that macrophages stimulated with Recombinant Gamma Interferon (rIFN-Gamma) produce tumor necrosis factor alpha (TNF-alpha), which in an autocrine fashion activates these cells. The aim of the present study was to determine whether endogenously formed TNF-alpha also is required for rIFN-Gamma-induced macrophage activation and enhanced antimicrobial activity in vivo. After an intraperitoneal injection of rIFN-Gamma into CBA/J mice, their peritoneal macrophages released enhanced amounts of NO2- and inhibited the intracellular proliferation of Toxoplasma gondii. Injection of neutralizing antibodies against TNF-alpha simultaneously with the rIFN-Gamma completely inhibited both the release of NO2- by macrophages and their toxoplasmastatic activity. Similar results were observed after intraperitoneal injection of a competitive inhibitor of L-arginine, NG-monomethyl-L-arginine, together with rIFN-Gamma, demonstrating that in vivo L-arginine-derived reactive nitrogen intermediates are essential for the induction of toxoplasmastatic activity. Intravenous injection of rIFN-Gamma inhibited the growth of Listeria monocytogenes in the livers and spleens of mice; this effect was abrogated by antibodies against TNF-alpha. Intravenous injection of a large dose of rTNF-alpha resulted in a decrease in the number of bacteria in the liver and spleen, but an injection of rIFN-Gamma and rTNF-alpha did not result in enhanced inhibition of the proliferation of L. monocytogenes. Together, the results of the present study are the first to demonstrate that endogenous TNF-alpha is required in vivo for the expression of macrophage activation with respect to the release of reactive nitrogen intermediates and toxoplasmastatic activity and for enhanced listericidal activity in the livers and spleens of mice stimulated with rIFN-Gamma.
E Park - One of the best experts on this subject based on the ideXlab platform.
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Mycobacterial lipoarabinomannan induces nitric oxide and tumor necrosis factor alpha production in a macrophage cell line: down regulation by taurine chloramine.
Infection and immunity, 1994Co-Authors: G B Schuller-levis, W R Levis, M Ammazzalorso, A Nosrati, E ParkAbstract:Avirulent mycobacterium H37Ra lipoarabinomannan (LAM) elicited nitric oxide (NO) and tumor necrosis factor alpha in a dose-dependent manner in a murine macrophage cell line, RAW 264.7 cells. H37Ra LAM and Recombinant Gamma Interferon were highly synergistic for NO production. The production of NO and the release of tumor necrosis factor alpha stimulated by H37Ra LAM plus Recombinant Gamma Interferon in RAW 264.7 cells are inhibited by taurine chloramine.
J. A. M. Langermans - One of the best experts on this subject based on the ideXlab platform.
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Endogenous tumor necrosis factor alpha is required for enhanced antimicrobial activity against Toxoplasma gondii and Listeria monocytogenes in Recombinant Gamma Interferon-treated mice.
Infection and immunity, 1992Co-Authors: J. A. M. Langermans, M. E. B. Van Der Hulst, P. H. Nibbering, R. Van FurthAbstract:In vitro studies have shown that macrophages stimulated with Recombinant Gamma Interferon (rIFN-Gamma) produce tumor necrosis factor alpha (TNF-alpha), which in an autocrine fashion activates these cells. The aim of the present study was to determine whether endogenously formed TNF-alpha also is required for rIFN-Gamma-induced macrophage activation and enhanced antimicrobial activity in vivo. After an intraperitoneal injection of rIFN-Gamma into CBA/J mice, their peritoneal macrophages released enhanced amounts of NO2- and inhibited the intracellular proliferation of Toxoplasma gondii. Injection of neutralizing antibodies against TNF-alpha simultaneously with the rIFN-Gamma completely inhibited both the release of NO2- by macrophages and their toxoplasmastatic activity. Similar results were observed after intraperitoneal injection of a competitive inhibitor of L-arginine, NG-monomethyl-L-arginine, together with rIFN-Gamma, demonstrating that in vivo L-arginine-derived reactive nitrogen intermediates are essential for the induction of toxoplasmastatic activity. Intravenous injection of rIFN-Gamma inhibited the growth of Listeria monocytogenes in the livers and spleens of mice; this effect was abrogated by antibodies against TNF-alpha. Intravenous injection of a large dose of rTNF-alpha resulted in a decrease in the number of bacteria in the liver and spleen, but an injection of rIFN-Gamma and rTNF-alpha did not result in enhanced inhibition of the proliferation of L. monocytogenes. Together, the results of the present study are the first to demonstrate that endogenous TNF-alpha is required in vivo for the expression of macrophage activation with respect to the release of reactive nitrogen intermediates and toxoplasmastatic activity and for enhanced listericidal activity in the livers and spleens of mice stimulated with rIFN-Gamma.
Hiromi Nagaoka - One of the best experts on this subject based on the ideXlab platform.
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Intractable Q fever treated with Recombinant Gamma Interferon.
The Pediatric infectious disease journal, 2001Co-Authors: Yutaka Morisawa, Hiroshi Wakiguchi, Tomoki Takechi, Takanobu Kurashige, Hiromi NagaokaAbstract:A 3-year-old boy with Q fever received several kinds of antibiotics including minocycline, but spiking fever and positive PCR of Coxiella burnetii continued for several months. He became asymptomatic and his abnormal laboratory data normalized after the administration of Gamma Interferon three times a week.
Julio A. Ramirez - One of the best experts on this subject based on the ideXlab platform.
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Inhibition of Chlamydia pneumoniae growth in HEp-2 cells pretreated with Gamma Interferon and tumor necrosis factor alpha.
Infection and immunity, 1995Co-Authors: James T. Summersgill, N N Sahney, C A Gaydos, T C Quinn, Julio A. RamirezAbstract:An in vitro culture system was used to study the effects of increasing concentrations of human cytokines on the intracellular replication of Chlamydia pneumoniae. HEp-2 cell monolayers, pretreated for 24 h with 200 U of human Recombinant Gamma Interferon (IFN-Gamma) per ml restricted the intracellular replication of C. pneumoniae. Tumor necrosis factor alpha (TNF-alpha; 25 ng/ml) exhibited a synergistic effect with IFN-Gamma by reducing the concentration of IFN-Gamma necessary to restrict intracellular growth to 100 U/ml. The addition of 200 micrograms of tryptophan per ml significantly reversed the inhibitory effects of IFN-Gamma and TNF-alpha, suggesting involvement of the indoleamine-2,3-dioxygenase pathway in the restriction process.