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PubMed1982

[Studies on the therapeutics of experimental toxoplasmosis. II. Effect of acetylspiramycin alone or in combination with an immunopotentiator (CSP-II) or sulfamethopyrazine on Toxoplasma multiplication in the heart of mice acutely and chronically infected with Toxoplasma gondii (author's transl)].

Normal mice acutely and chronically infected with the S-273 strain of T. gondii, were treated with acetylspiramycin (ASPM) alone, 8 mg/mouse/day, per os, or in combination with an immunopotentiator (CSP-II), 10 mg/mouse/day, intraperitoneally, or sulfamethopyrazine (SMPZ), 2 mg/mouse/day, per os, for a period of 4 weeks. In the acute cases, a 99.4% cyst reduction was obtained with ASPM alone and no cysts were seen in the brains of mice treated with ASPM in combination with CSP-II or SMPZ. The organisms were significantly eradicated in the brain and heart tissues of mice treated with ASPM alone or in combination with CSP-II or SMPZ as shown by subinoculation to normal mice and the negative latex hemagglutination titers of the recipient mice. In the chronic cases, a cyst reduction of 52.4% was obtained with mice treated with ASPM in combination with CSP-II. A cyst reduction of 34.6%, 32.9% and 20.8% was obtained in the ASPM alone, CSP-II alone and ASPM in combination with SMPZ treated groups, respectively. A comparative clearing of the organisms in the heart tissues of mice treated with ASPM in combination with CSP-II was obtained compared to the other treatment groups but not in the brains of all groups.

Adjuvants, Immunologic↗
PubMed1970

The Toxoplasma gondii oocyst from cat feces.

Coccidian oocysts resembling those of Isospora bigemina were excreted by cats fed Toxoplasma. In order to identify these oocysts with Toxoplasma infectivity a number of critical comparisons were made. The appearance of oocysts and Toxoplasma infectivity was simultaneous in the feces of 23 of 24 adult cats, 3-5 days after feeding of Toxoplasma cysts; in the feces of 4 out of 9 cats, 7-10 days after feeding of trophozoites; and in 8 out of 17 cats, 20-24 days after feeding of cat feces containing oocysts. Oocysts and infectivity were present in similar numbers, and they disappeared simultaneously from the feces of cats. Oocysts and infectivity were also observed simultaneously in the feces of 9 kittens, 1-2 days old, fed Toxoplasma cysts. Oocysts could not be separated from infectivity by filtration, by continuous particle electrophoresis, or by density gradient centrifugation. Excystation of oocysts was followed by an increase in titer of Toxoplasma infectivity. Unsporulated oocysts in fresh cat feces were noninfectious to mice, but oocyst sporulation was associated quantitatively with the development of infectivity at different temperatures and conditions of oxygenation. Maximum oocyst sporulation at 48 hr correlated with the development of maximum Toxoplasma infectivity. 1 and 2% sulfuric acid, and 2.5% potassium dichromate were found to be the best preservatives for sporulation of oocysts and for the development of Toxoplasma infectivity. Low sporulation rates in 0.1% formalin, 20% ethanol, and in water were associated with low infectivity in these reagents. Neither Toxoplasma infectivity nor oocysts developed in 0.3% formalin, 1% ammonium hydroxide, or 1% iodine in 20% ethanol. Oocysts, sporocysts, and sporozoites were stained specifically with Toxoplasma antibody in the indirect fluorescent antibody test. Typical coccidian stages, schizonts, and male and female gametocytes were found in the epithelium of the small intestine of kittens fed Toxoplasma cysts. The classification of T. gondii is discussed in relation to that of other isosporan coccidia of cats and dogs. The term "Toxoplasma oocyst" is introduced and Toxoplasma is classified in the family Toxoplasmidae of the suborder Eimeriina. The species Isospora bigemina is restricted to dogs, and I. cati to cats. I. felis and so-called I. rivolta from cats were noninfectious to dogs, and did not confer immunity to subsequent infection with I. canis and I. rivolta from dogs.

Air↗
PubMed1987

Unique differences in infectivity and seroreactivity of Toxoplasma harvested from mice infected for different lengths of time.

For use in experiments, Toxoplasma of the RH strain are usually harvested from mouse peritoneal cavities 48 hr (2-day Toxoplasma) or more after intraperitoneal inoculation. In this report we show that Toxoplasma harvested at 24 hr (1-day Toxoplasma) after inoculation are much more infective for and replicate to a greater degree within mouse resident peritoneal macrophages in vitro and are much more resistant to the cidal activity of activated mouse peritoneal macrophages and resident rat peritoneal macrophages than are 2-day Toxoplasma. Ingestion of 1-day Toxoplasma by macrophages did not trigger the respiratory burst as measured by reduction of nitroblue tetrazolium (NBT), but coating 1-day Toxoplasma with specific antibody did result in reduced NBT. However, coating 1-day Toxoplasma with specific antibody did not markedly decrease infectivity for macrophages in vitro, unlike decreased infectivity observed when 2-day Toxoplasma are coated with specific antibody. Use of 1-day Toxoplasma in the dye test resulted in a 5-fold decrease in titer of specific antibody in human sera. Use of Toxoplasma harvested 24 hr after infection may serve as a new tool to probe virulence factors of Toxoplasma and of host cells' antimicrobial mechanisms.

Animals↗
PubMed1996

CD4-mediated and CD8-mediated cytotoxic and proliferative immune responses to Toxoplasma gondii in seropositive humans.

Both CD4+ and CD8+ cytotoxic T lymphocytes (CTL) are part of the human immune response to Toxoplasma gondii infection. To further our understanding of Toxoplasma immunity, we investigated factors influencing stimulation of CD4+ or CD8+ human T. gondii-specific immune cells. Both antigen-pulsed and Toxoplasma-infected antigen-presenting cells (APC) induced cell proliferation. Toxoplasma-infected APC elicited strong proliferation of CD4+ cells, but little or no proliferation of CD8+ cells, unless high antigen loads were used. Toxoplasma-infected APC stimulated specific cytotoxicity poorly or not at all, owing to death of stimulated cultures, whereas antigen-pulsed APC strongly elicited specific cytotoxicity. Cytotoxicity elicited by either type of APC resided exclusively in CD4+ T cells in polyclonal cultures. Thus, Toxoplasma-infected APC elicited stronger CD4-mediated than CD8-mediated cell proliferation and generated CD4+ CTL more readily than CD8+ CTL. Nonetheless, specific CD8+ memory cells were demonstrated, and rare CD8+ Toxoplasma-specific CTL were subcloned. Fixed Toxoplasma-infected APC (which induce CD8+ CTL) also elicited cell proliferation, but polyclonal cultures stimulated with these infected APC did not die. Unfixed Toxoplasma-infected APC strongly inhibited phytohemagglutinin-induced cell proliferation, whereas fixed APC did not. These data suggested that infected APC were inhibitory or lethal to some immune cells. Further investigations into interactions between immune cells and Toxoplasma-infected cells likely will help elucidate factors involved in the immunopathogenesis of Toxoplasma infection. As other intracellular parasites, including Plasmodium spp. and Leishmania spp., also elicit CD4+ CTL, such work may help establish paradigms governing immunity to intracellular parasites.

Animals↗
PubMed2000

[Toxoplasma pericarditis without immunosuppressant disorder detected by polymerase chain reaction of pericardial fluid: a case report].

There have been several case reports, a total of 22 up to the present, of toxoplasma pericarditis. Out of them, in only a few cases the diagnosis was properly made with a proof of the microscopic presence of Toxoplasma gondii. This is the first report of toxoplasma pericarditis in which the presence of Toxoplasma gondii was detected by polymerase chain reaction of pericardial effusion. In addition, the previous reports will be reviewed, and compared to this present case. A 29-year-old woman, without immunosuppressant disorder, suffering from fever and orthopnea was admitted to our hospital. Blood chemistry findings indicated mild liver dysfunction and inflammation. Chest radiography showed cardiac enlargement. Electrocardiography showed sinus tachycardia and ST elevation. Echocardiography revealed a massive pericardial effusion. Pericardiocentesis demonstrated 638 ml of bloody fluid. Cytologic study of the fluid was class II for malignancy, and polymerase chain reaction to tuberculosis was negative. However, a high titer of the anti-toxoplasma antibody of 1: 20,480 (passive hemagglutination) indicated pericarditis caused by Toxoplasma gondii. Subsequently, Toxoplasma gondii was identified in the pericardial effusion by polymerase chain reaction. Clinical symptoms improved after pericardiocentesis, but 2 months later pericarditis recurred. Treatment was started with 800 mg acetylspiramycin daily but failed to improve the symptoms. Because of the development of pleuritis, treatment was changed to sulfadoxine 1,000 mg/pyrimethamine 50 mg. After the treatment with them, her symptoms improved. Only 22 cases of toxoplasma pericarditis have been reported worldwide and 15 of those cases were without immunosuppressant disorder. The usual symptoms at the onset of pericarditis without immunosuppressant disorder are fever, dyspnea and chest pain. Seven patients developed cardiac tamponade. Pericardiocentesis was performed in 8 cases and the pericardial fluid was hemorrhagic in 6. Pericardial thickening was detected in 5 cases. The diagnosis of toxoplasma infection is very difficult, because asymptomatic infection of Toxoplasma gondii is very common. Pericarditis is a disease difficult to confirm the etiology. Detection of Toxoplasma gondii in pericardial effusion by the polymerase chain reaction is very useful for its diagnosis.

Adult↗
PubMed1984

Cellular defenses against Toxoplasma gondii in newborns.

Mononuclear phagocytes, particularly macrophages (M phi) that have been activated by lymphokines, are the principal defense against intracellular pathogens such as Toxoplasma gondii. To determine reasons for the newborns' susceptibility to Toxoplasma infection, we compared: the interaction of Toxoplasma with newborns' mononuclear phagocytes (blood monocytes and two types of newborn M phi, those derived from blood monocytes or from placental tissue) with adults' blood monocytes and monocyte-derived M phi and the production of M phi-activating lymphokines (MAF) by Concanavalin A (ConA)-stimulated newborn and adult blood mononuclear cells (MC). Newborn and adult monocytes killed Toxoplasma with equal efficiency. Similarly, survival and replication of Toxoplasma were comparable in control newborn and adult M phi. Exposure to adult ConA supernatants significantly decreased the survival and replication of Toxoplasma both in adult and newborn M phi. In contrast, exposure to cord blood ConA supernatants failed to affect the survival or the replication of Toxoplasma in newborn M phi and decreased the replication but not the survival of Toxoplasma in adult M phi. Exposure to ConA supernatants of peripheral blood MC from 2-5-d old newborns failed to affect survival or replication of Toxoplasma in newborn or adult M phi. Thus, both generation of MAF by newborn blood MC and response to newborn MAF by newborn M phi were impaired. Generation of MAF by adult blood mononuclear cells was not inhibited by cord blood MC nor was generation of MAF by cord blood MC increased by depletion of OKT8 antibody-binding cells, by depletion of adherent cells with or without addition of adult adherent cells, or by addition of indomethacin. Depletion of OKT4 antibody-binding cells abrogated the generation of MAF both by adult and cord blood MC. The activity of adult ConA supernatants was abrogated by dialysis at pH 2 or by addition of anti-gamma-interferon but not anti-alpha-interferon antibody. However, the correlation between antiviral interferon activity and anti-Toxoplasma activity was weak (r = 0.40). Enhanced M phi anti-Toxoplasma activity was not associated with detectably enhanced superoxide anion generation, nitroblue tetrazolium reduction, or phagolysosome fusion, and was not inhibited by catalase, superoxide dismutase, or mannitol. These results indicate that generation of and response to MAF is decreased in cells from human newborns and that gamma-interferon may be the major MAF under these conditions.

Adult↗
PubMed1994

Effects of cytokines in the activation of peritoneal macrophages from mice infected with Toxoplasma gondii.

The present study was undertaken to assess the role of cytokines in the activation of peritoneal macrophages from Toxoplasma-infected mice. Peritoneal macrophages from Toxoplasma-infected mice (10 cysts of Beverley strain/mouse) were harvested 8 weeks after infection, and incubated with the mitogen-induced lymphokine, recombinant mouse interferon-gamma (IFN-gamma), recombinant mouse tumor necrosis factor-alpha (TNF-alpha) alone or in combination with IFN-gamma (IFN-gamma/TNF-alpha) for 24 hr at 37 degrees C, 5% CO2. Macrophage activation was measured by the amount of H2O2 and NO2- production, and anti-Toxoplasma activities of macrophages. IFN-gamma or IFN-gamma/TNF-alpha-treated macrophages from Toxoplasma-infected mice revealed significantly higher H2O2 production than resident macrophages from Toxoplasma-infected mice. The production of NO2- by TNF-alpha-, IFN-gamma- or IFN-gamma/TNF-alpha-treated macrophages from Toxoplasma-infected mice were significantly higher than that by resident macrophages, whereas lymphokine-treated group produced similar amount as that produced by resident macrophages. Anti-Toxoplasma activities of cytokine-treated macrophages from Toxoplasma-infected mice were significantly higher than those of resident macrophages. IFN-gamma-treated macrophages were significantly increased production of H2O2 and NO2-, and anti-Toxoplasma activities of macrophages between normal and Toxoplasma-infected mice, whereas the other cytokine-treated groups were not significant differences between them. These data suggested that IFN-gamma was the only one of cytokines capable of significantly activating the peritoneal macrophages from Toxoplasma-infected mice.

Animals↗
PubMed1986

The effects of cyclosporine on Toxoplasma gondii in vivo and in vitro.

We examined the effect of cyclosporine on Toxoplasma infection in vivo and in vitro. Administration to mice of 150 mg/kg/day cyclosporine variably affected mortality in four separate experiments. IgG (Sabin-Feldman dye test) and IgM enzyme-linked immunosorbent assay antibody titers were significantly depressed in mice treated with cyclosporine. These results suggested the possibility that cyclosporine possesses anti-Toxoplasma activity. Thus, macrophages were incubated with cyclosporine before and after infection with Toxoplasma. Treatment with 0.5, 1, and 5 micrograms cyclosporine/ml during or after challenge of macrophage monolayers with Toxoplasma inhibited replication of Toxoplasma (and resulted in killing of Toxoplasma). The effect of cyclosporine on development of activated macrophages was studied. Cyclosporine administered to mice at a dose of 150 mg/kg/day neither accelerated nor delayed activation of macrophages (assessed by inhibition of Toxoplasma replication in vitro) by i.v. injection of either Corynebacterium parvum or Toxoplasma. Cyclosporine affects mortality variably in murine toxoplasmosis, depresses synthesis of IgG and IgM Toxoplasma antibody in vivo, does not prevent activation of macrophages in vivo, and possesses anti-Toxoplasma activity in vitro and perhaps in vivo. Cyclosporine may be the preferred immunosuppressive agent for recipients of an organ transplant who are at high risk for toxoplasmosis (e.g., seronegative recipients who have received organ from seropositive donors).

Animals↗
PubMed1979

Longitudinal studies of lymphocyte response to Toxoplasma antigen in humans infected with T. gondii.

Toxoplasma antigen-specific lymphocyte transformation was measured in subjects in whom the diagnosis of acute acquired Toxoplasma infection was documented and in whom the time of onset of clinical illness was carefully determined. Neither false positive nor false negative reactions to Toxoplasma antigen were seen in lymphocytes from uninfected subjects or subjects with chronic Toxoplasma infection. Lymphocytes from subjects in both of these control groups responded equally to a different antigen, streptokinase-streptodornase (SK/SD). On the initial determination, the lymphocytes of 7 of 24 subjects with acute Toxoplasma infection of less than 12 months' duration failed to transform to Toxoplasma antigen. Five of these 7 subjects were among a group of 14 who had developed clinical illness less than 3 months previously. To determine when lymphocyte transformation to Toxoplasma antigen developed, longitudinal studies were carried out in subjects with acute Toxoplasma infection whose lumphocytes failed to transform initially to Toxoplasma antigen. It was found that in all patients, lymphocytes transformed with Toxoplasma antigen eventually, though in two patients this occurred between 9 and 12 months after the initial infection.

Adolescent↗
PubMedDate not supplied

Phagosome acidification blocked by intracellular Toxoplasma gondii.

Toxoplasma gondii belongs to a group of highly virulent intracellular parasites that reside in host cell vacuoles which resist typical phagosome-lysosome fusion. Live Toxoplasma replicate prodigiously within modified phagocytic vacuoles formed during invagination of the host plasma membrane. In contrast, heat-killed Toxoplasma or specific antibody (heat-inactivated)-coated live Toxoplasma-containing vacuoles readily undergo lysosome fusion and digestion in normal macrophages. Of newly recognized significance to Toxoplasma survival is the microbicidal effect of phagosome acidification, which reportedly can occur independently of fusion with other acidic vesicles. We report here that modified live Toxoplasma-containing vacuoles fail to acidify in normal macrophages, as indicated by the sensitive pH probe fluorescein. In contrast, when live Toxoplasma are coated with specific antibody (heat-inactivated), they trigger phagosome acidification when entering normal macrophages. A similar acidification is observed when normal phagocytes ingest dead Toxoplasma. Extracellular Toxoplasma are highly susceptible to acidic pH conditions, indicating that the acidification block in the modified vacuoles may be important for intracellular survival.

Animals↗
PubMed1986

Toxoplasma modifies macrophage phagosomes by secretion of a vesicular network rich in surface proteins.

Modification of macrophage phagosomes begins shortly after formation as Toxoplasma cells secrete membranous vesicles that form a reticulate network within the vacuole. The Toxoplasma-modified compartments then resist normal endocytic processing and digestion. We have used the pronounced Ca++-dependent stability of the intraphagosomal membrane (IPM) network to purify and characterize the structural proteins of this assembly. In addition to the structural matrix, Toxoplasma secretes a discrete set of soluble proteins, including a newly described 22-kD calcium-binding protein. The IPM network adheres to intact Toxoplasma cells after host cell lysis in the presence of 1 mM Ca++; however, the network readily disperses in calcium-free buffer and was purified as vesicles that sedimented at 100,000 g. Purified IPM vesicles were specifically recognized by immune sera from mice with chronic Toxoplasma infection and consisted primarily of a 30-kD protein when analyzed by SDS PAGE. IPM network proteins share a major antigenic component located on the surface of extracellular Toxoplasma cells as shown by immunoperoxidase electron microscopy using a polyclonal antibody prepared against the IPM vesicles. Moreover, in Toxoplasma-infected macrophages, anti-IMP antibody confirmed that the extensive IPM array contains proteins also found on the Toxoplasma cell surface. Our results indicate the IMP network represents a unique structural modification of the phagosome comprised in part of Toxoplasma surface proteins.

Animals↗
PubMed1972

The interaction between Toxoplasma gondii and mammalian cells. II. The absence of lysosomal fusion with phagocytic vacuoles containing living parasites.

Electron microscope methods have been used to study delivery of macrophage primary or secondary lysosomal contents to phagocytic vacuoles containing living or dead toxoplasmas. Secondary lysosomes were labeled by culturing the cells in colloidal thorium dioxide (thorotrast) or in ferritin. Acid phosphatase cytochemistry was employed for detection of primary as well as secondary lysosomal constituents. These various lysosomal labels were present in nearly all vacuoles containing toxoplasmas killed with glutaraldehyde, or in vacuoles containing those parasites undergoing degeneration 1 hr after the uptake of living toxoplasmas. In contrast, at times ranging from 1 to 20 hr after infection, no vacuoles containing morphologically normal, apparently viable toxoplasmas were thorotrast or ferritin positive, and only rarely did these vacuoles react for acid phosphatase. In many instances vacuoles containing viable toxoplasmas and no lysosomal markers were situated in the same cell nearby to vacuoles containing degenerating toxoplasmas and lysosomal constituents, thus indicating that the determinants of lysosomal fusion were operating locally in the immediate vicinity of the phagocytic vacuole, and not operating to influence general cell function. Thus, some toxoplasmas are able to prevent the delivery of lysosomal contents, and apparently the phagocytic vacuole provides for these parasites a sheltered microenvironment ideal for their growth. Morphologic evidence indicated that living toxoplasmas altered the phagocytic vacuolar membrane in macrophages, fibroblasts, and HeLa cells. Within minutes after phagocytosis, the vacuole became surrounded by closely apposed strips of endoplasmic reticulum and mitochondria; somewhat later, microvillous protrusions of the membrane into the vacuole were seen. These morphologic features of phagocytic vacuoles containing living toxoplasmas may be of importance in relation to the absence of lysosomal fusion, or they may serve some function in protecting the host cell or in nourishing the parasite.

Acid Phosphatase↗
PubMed1974

Effect of normal and activated human macrophages on Toxoplasma gondii.

Human macrophages derived from in vitro culture of peripheral blood monocytes were studied under a variety of conditions to determine their microbicidal capacity for the obligate intracellular protozoan, Toxoplasma gondii. The effect of macrophages on intracellular Toxoplasma was evaluated morphologically by light and phase microscopy and by autoradiography. When macrophages from dye test (DT)-negative or DT-positive individuals were infected with Toxoplasma in the presence of normal human serum, the organisms were able to multiply intracellularly with resultant destruction of the monolayer. Once organisms were intracellular, the presence of antibody-containing serum in the medium did not alter this inability of the macrophages to kill Toxoplasma. However, when Toxoplasma were incubated in the presence of heat-inactivated DT-positive serum just before infection of the monolayers, the intracellular organisms were inhibited or killed by normal macrophages. Attempts were made to activate macrophages in vitro to kill Toxoplasma. Macrophages incubated in the presence of sensitized lymphocytes and Streptokinase-Streptodornase (SK-SD) or Toxoplasma lysate antigen (TLA) were found to kill Toxoplasma when compared to macrophages incubated in the presence of lymphocytes from DT-negative individuals and TLA or lymphocytes alone. Thus, in vitro induction of resistance (both specifically and nonspecifically) in human macrophages was accomplished by culturing these cells in the presence of specifically sensitized lymphocytes and antigen. These results suggest that, as in the mouse model, activated human macrophages have the ability to inhibit or kill intracellular Toxoplasma and that these cells may be important as effector cells in cell-mediated immunity (CMI) to toxoplasmosis in man.

Adolescent↗
PubMed1975

Inhibition of multiplication of Toxoplasma gondii by human monocytes exposed to T-lymphocyte products.

The multiplication of Toxoplasma gondii was quantitated in human monocytes in vitro by phase-contrast microscopy. Toxoplasma multiplication was identical in monocytes from subjects byt was significantly inhibited in cells from both sources if the monocytes were preincubated with immune lymphocytes and toxoplasma monocytes were preincubated with immune lymphocytes and toxoplasma antigen. Supernates prepared from toxoplasma-immune lymphocytes incubated with toxoplasma antigen were also effective in inducing in monocytes the capacity to inhibit toxoplasma multiplication. Supernative acitivty was evident after lymphocytes and antigen were incubated for as little as 15 min. The instruction of monocytes was also repid and reversible. Monocytes were fully induced to inhibit toxoplasma multiplication after a 2 h exposure to an active supernate, but they lost their inhibitory capacity on culture in vitro for 48 h in the absece of immune cells or their products. The lymphocytes particupating in the monocyte induction were identified as t cells. The in vitro stimulation of monocytes appeared to exhibit some specificity, since no inhibition of toxopreotein derivative and lymphocytes from tuberculin-positive subjects, concanavalin a-stimulated lymphocytes, or their supermates. Supernates which induced monocytes to inhibit toxoplasma multiplication did not influence parasite growth in HeLa cells.

Adult↗
PubMed2003

Uptake of nitrobenzylthioinosine and purine beta-L-nucleosides by intracellular Toxoplasma gondii.

Intracellular Toxoplasma gondii grown in human foreskin fibroblast cells transported nitrobenzylthioinosine [NBMPR; 6-[(4-nitrobenzyl)mercapto]-9-beta-D-ribofuranosylpurine], an inhibitor of nucleoside transport in mammalian cells, as well as the nonphysiological beta-L-enantiomers of purine nucleosides, beta-L-adenosine, beta-L-deoxyadenosine, and beta-L-guanosine. The beta-L-pyrimidine nucleosides, beta-L-uridine, beta-L-cytidine, and beta-L-thymidine, were not transported. The uptake of NBMPR and the nonphysiological purine nucleoside beta-L-enantiomers by the intracellular parasites also implies that Toxoplasma-infected cells can transport these nucleosides. In sharp contrast, under the same conditions, uninfected fibroblast cells did not transport NBMPR or any of the unnatural beta-L-nucleosides. beta-D-Adenosine and dipyridamole, another inhibitor of nucleoside transport, inhibited the uptake of NBMPR and beta-L-stereoisomers of the purine nucleosides by intracellular Toxoplasma and Toxoplasma-infected cells. Furthermore, infection with a Toxoplasma mutant deficient in parasite adenosine/purine nucleoside transport reduced or abolished the uptake of beta-D-adenosine, NBMPR, and purine beta-L-nucleosides. Hence, the presence of the Toxoplasma adenosine/purine nucleoside transporters is apparently essential for the uptake of NBMPR and purine beta-L-nucleosides by intracellular Toxoplasma and Toxoplasma-infected cells. These results also demonstrate that, in contrast to the mammalian nucleoside transporters, the Toxoplasma adenosine/purine nucleoside transporter(s) lacks stereospecificity and substrate specificity in the transport of purine nucleosides. In addition, infection with T. gondii confers the properties of the parasite's purine nucleoside transport on the parasitized host cells and enables the infected cells to transport purine nucleosides that were not transported by uninfected cells. These unique characteristics of purine nucleoside transport in T. gondii may aid in the identification of new promising antitoxoplasmic drugs.

Animals↗