Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMEBICIDES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1989

Cytokine activation of murine macrophages for in vitro killing of Entamoeba histolytica trophozoites.

Macrophage-mediated effector mechanisms against the protozoan parasite Entamoeba histolytica were studied. Unstimulated macrophages were inefficient at killing E. histolytica trophozoites in vitro and were killed by the trophozoites. Conversely, immature cells of the mononuclear phagocyte lineage (promonocytes) were shown to display a strong spontaneous amebicidal activity. The acquisition of macrophage amebicidal activity following cytokine treatment was investigated. Gamma interferon, tumor necrosis factor alpha, and macrophage colony-stimulating factor 1, or combinations thereof, were shown to endow murine bone marrow-derived macrophages with significant amebicidal activity. Low doses of gamma interferon and tumor necrosis factor alpha and of gamma interferon and colony-stimulating factor 1 were shown to act synergistically in this phenomenon. This enhancement of amebicidal activity was shown to operate on bone marrow-derived macrophages, elicited peritoneal macrophages, and, to a much lesser extent, spleen macrophages. Although acquisition of amebicidal activity was associated with a strong respiratory burst, the addition of oxygen-free radical scavengers showed that the killing activity was approximately 45% H2O2 dependent. In addition, amebicidal activity by macrophages was shown to be contact dependent and was inhibited by 61% with the protease inhibitor tosyl lysyl chloromethyl ketone. Our results indicate that immunologic production of gamma interferon, tumor necrosis factor alpha, and colony-stimulating factor 1 could be important in the activation of macrophages for host defense against amebiasis and that promonocytes are strong effector cells against virulent amebae.

Amebicides↗
PubMed1969

Virulence Of Entamoeba Histolytica According To The Strains In Korea: III. Amebicial Response Of Antiamoebic Agents On Several Strains Of Entamoeba Histolytica In Vitro.

The amebicidal activity of traditional anitiamoebic drug (emetine, carbasone, diodoquin, chloroquine, atabrine, chloramphenicol and tertracycline) and newly appeared chemicals(niridazole, metronidazole and No. 8603 substance) were assayed by in vitro experiment using five strains of human originated E, histolytica. The variety of amebicidal activity of drugs by the strains were discussed. 1)Ranges of amoebicidal activity of traditional antiamoebic drugs kept almost similar titers of previous reports at the concentration; 1:5,000 to 1:20,000 with emetine hydrochloride, 1:10.000 to 1:20,000 with carbarsone, 1:8,000 to 1:16,000 with diodoquin, 1:50,000 with chloroquine, 1:1,000 to 1: 4,000 with atabrine,1:1,000 to 1:2,000 with chloramphencol and 1:5,000 to 1:8,000 with tetracycline. The newly appeared chemicals showed higher amebicidal titres at the concentration; 1:500,000 to 1:5,000,000 with niridazole, 1:50,000 to 1:100,000 with metronidazol and 1:100,000 to 1:500,000 with No.8603 substance. 2)Emetine, chloramphenicol and No. 8603 substance showed amebicidal activities at lower concentration to intestine originated amebae (YS 14, YS 15 and NAMRU II strain) than to liver originated amebae (YS 24 and YS 25 strain), while carbarsone, chloroquine and metronidazole showed the activity at higher concentrations. Diodoquin showed lower amebicidal titres to trophozoite borne amebae (NAMRU II, YS 24 and YS 25 strain) than to cyst borne amebae(YS 14 and YS 15 strain), but niridazole showed converse results. The concentration of atabrine for amebicidal activity was not constant according to strains of the amoeba, but tetracycline showed almost settled titers.

Journal Article↗
PubMed1992

Macrophage cytotoxicity against Entamoeba histolytica trophozoites is mediated by nitric oxide from L-arginine.

The killing of Entamoeba histolytica trophozoites by phagocytes involves oxidative and nonoxidative mediators. In this study, we determine whether L-arginine-derived nitric oxide (NO) is involved in the killing of E. histolytica trophozoites by activated murine macrophages in vitro. Elicited peritoneal and bone marrow-derived macrophages activated with IFN-gamma alone or with IFN-gamma and LPS killed 62 to 73% of amebae, concomitant with increased levels of nitrate (NO2). Depletion of L-arginine by addition of arginase to culture medium abrogated macrophage amebicidal activity. NG-monomethyl L-arginine, an L-arginine analog, competitively inhibited NO2 release and amebicidal activity in a dose-dependent fashion, without affecting H2O2 production; however, the addition of excess L-arginine competitively restored macrophage amebicidal effects. In culture, sodium nitrite and sodium nitroprusside were cytotoxic to E. histolytica and this was reversed by the addition of myoglobin. Exogenously added FeSO4 prevented macrophage cytotoxicity. Addition of superoxide dismutase, a scavenger of O2-, partially inhibited amebicidal activity, without influencing NO2 production. Untreated and LPS-exposed macrophages produced high levels of H2O2 independent from NO2 production and amebicidal effects. However, the addition of catalase, a scavenger of H2O2, inhibited both amebicidal activity and NO2 production by activated macrophages. Our results demonstrate that NO is the major cytotoxic molecule released by activated macrophages for the in vitro cytotoxicity of E. histolytica and that O2- and H2O2 may be cofactors for the NO effector molecule.

Animals↗