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F Kierszenbaum

Publications and source records attributed to F Kierszenbaum.

18 recordsLinked to original sources
PubMed1979

Thymus-dependent control of host defense mechanisms against Trypanosoma cruzi infection.

Congenitally athymic homozygous (nu/nu) mice were shown to be significantly more susceptible to Trypanosoma cruzi infection than their thymus-bearing heterozygous (nu/+) littermates, as measured by increased parasitemia, mortality rate, and shortened survival time. In addition, transplantation of neonatal thymus into athymic mice reestablished normal levels of resistance to T. cruzi, i.e., comparable to those of normal littermates. These results constitute conclusive evidence that host defense mechanisms active in experimental Chagas' disease are under thymic control.

Animals↗
PubMed1979

Antibody-dependent killing of bloodstream forms of Trypanosoma cruzi by human peripheral blood leukocytes.

Bloodstream forms of Trypanosoma cruzi were found to be destroyed by human lymphoid cells, neutrophils, or eosinophils in the presence of specific antibodies. Nonspecific immunoglobulins present in normal serum did not mediate the cytotoxic reaction. Cells or antibody had no significant lytic effect on the parasite when tested separately and purified, non-activated human adherent cells were inactive antibody was present or not.

Animals↗
PubMed1977

Cytotoxic effects of normal sera on lymphoid cells. II. Requirements for inhibition of nonspecific serum cytotoxicity by agarose.

Agarose is known to inhibit nonspecifically the cytotoxic effects of normal sera on xenogeneic lymphoid cells. To find an explanation for this agarose effect we have studied its requirements using guinea pig and human sera as the source of activity and rat thymocytes as target cells. Control assays were performed using heat-inactivated (56 C, 30 min) normal rat serum. The inhibitory effect of agarose was readily reproduced with untreated sera and also when sodium ethyleneglycoltetraacetate, a selective chelator of calcium ions, was added to the sera together with excess magnesium. However, the agarose effect failed to occur in the presence of 0.01 M EDTA unless magnesium ions were restored. Abrogation of cytotoxicity in human serum by incubation with a large number of target cells instead of agarose was also found to be magnesium dependent. Titrations of human serum, performed after absorption with agarose in the presence of EDTA, which does not interfere with antigen-antibody binding, and subsequent restoration of divalent cations, revealed no significant change in its cytotoxic titer when compared with that of mock-absorbed serum not subjected to the agarose treatment. Incubation of human serum with either agarose or rat thymocytes resulted in the conversion of factor B, essential for complement activation via the alternative pathway, previously shown to provide the complement activity necessary for the cytotoxic reaction. These results suggest that the agarose effect is mainly attributable to complement consumption via the alternative pathway rather than to the absorption of "natural" antibodies.

Animals↗
PubMed1977

Antibody-independent activation of the alternative complement pathway in human serum by parasitic cells.

The lysis of the monocellular parasite Trypanosoma cyclops by normal human serum (NHS) was found to be complement-dependent and to follow activation of the alternative pathway without apparent requirement for conventional antibodies. Lysis of the organisms was inhibited by heat-inactivating NHS at 56 degrees, preincubation of NHS with cobra venom factor or chelation of divalent cations with EDTA. It took place, however, in human C2-deficient serum and was inhibited by prior heating of NHS at 52 degrees to destroy the activity of factor B of the alternative pathway. Moreover, the lytic reaction was magnesium- but not calcium-dependent. Repeated low-temperature (0 degrees) absorption of either human hypogammaglobulinaemic serum or NHS with the parasite failed to remove or significantly decrease their lytic activities.

Complement System Proteins↗
PubMed1976

Mechanisms of natural resistance to trypanosomal infection. Role of complement in avian resistance to Trypanosoma cruzi infection.

The natural resistance of chickens to Trypanosoma curzi infection and the capacity of their sera to lyse blood (trypomastigote) forms of the parasite in vitro were found to be complement-dependent phenomena. Parasites given intravenously to decomplemented chickens were detectable in their bloodstream for at least 24 h post-infection, whereas in untreated animals they became undetectable after 1 min (and destroyed flagellates were observed). One millilitre of serum had the capacity to lyse as many as 10-30 X 10(6) organisms. The lytic activity of serum in vitro was not impaired in chickens that had been immunosuppressed by four different procedures and was present in the absence of antibodies. In vitro lysis of T. cruzi by either normal or antibody-free chicken sera occurred in the absence of calcium ions but required magnesium ions, indicating that complement was activated via the alternative pathway. Administration of normal chicken serum to mice infected with T. cruzi provoked a marked decrease in their parasitaemias.

Animals↗
PubMed1976

Mechanisms of resistance against experimental Trypanosoma cruzi infection: the importance of antibodies and antibody-forming capacity in the Biozzi high and low responder mice.

The role of antibodies and the host's antibody-forming capacity in resistance to Trypanosoma cruzi infection has been investigated in the Biozzi high and low responder lines of mice. Ab/L animals with low antibody-forming capacity were found to be more susceptible to i.p. infection with trypomastigotes than high responders (Ab/H), whereas non-selected Swiss albino mice showed an intermediate level of susceptibility. The correlation between antibody-forming potentiality and susceptibility was consistently observed with both the Y and Tulahuén strains of the parasite, which differ in their preferential tissue tropism as well as virulence. A similar divergence in susceptibility was observed after subcutaneous infection with the Y strain which produced a more fulminating disease. Although Ab/L mice neither produced a significant antibody response to the parasite nor responded to prophylactic immunization with killed T. cruzi epimastigotes, they could be effectively protected by passive transfer of immune plasma.

Animals↗
PubMed1975

Effects of complement depletion in experimental chagas disease: immune lysis of virulent blood forms of Trypanosoma cruzi.

In mice infected with virulent blood (trypomastigote) forms of Trypanosoma cruzi, complement depletion with cobra venom factor caused a marked exacerbation of the disease evidenced by significantly increased parasitemia levels and early mortality as compared with those of untreated infected animals. The effect was greater in mice receiving cobra venom factor on day 7 postinfection, i.e., at the time when the parasites had had time to localize and multiply in the tissues and appeared in the circulation in appreciable numbers. The possibility that complement participates in host defense against T. cruzi infection through a mechanism involving immune lysis was explored in vitro. T. cruzi trypomastigotes were found to undergo immune lysis in sera of patients with chronic Chagas' disease, in sera of immunized mice, and in solutions containing both immune mouse gamma globulin and a source of active complement. This phenomenon failed to take place either in the absence of complement or after complement inactivation by heat or utilizing complement inactivators. The lytic capacity of heated sera was restored by the addition of active complement to the system. During the immune lysis of T. cruzi blood forms, complement was activated in human sera via both the classical and the alternate pathways. In mouse sera, activation followed at least the alternate pathway.

Animals↗
PubMed1975

Immunization against experimental Chagas' disease by using culture forms of Trypanosoma cruzi killed with a solution of sodium perchlorate.

Protection against infection with virulent blood (trypomastigote) forms of Trypanosoma cruzi was accomplished in mice by immunization with culture (mainly epimastigote) forms killed by treatment with sodium perchlorate. Sodium chloride, used instead of sodium perchlorate, with all other conditions kept the same, failed to kill all the organisms, indicating that the effects of the perchlorate anion were not simply ionic or osmotic, suggesting that they might be chaotropic. A single dose of the immunogen, without adjuvants, was sufficient to significantly protect against the infection. Protection was achieved by either intraperitoneal, intramuscular, or subcutaneous immunization, though the first two routes appeared to be more effective. After challenge, parasitemias were negative in 25, 29, and 17% of the animals immunized intraperitoneally, intramuscularly, and subcutaneously, respectively.

Animals↗
PubMed1975

Enhancement of resistance and suppression of immunization against experimental Trypanosoma cruzi infection by Corynebacterium parvum.

Intravenous but not intraperitoneal injection of killed Corynebacterium parvum either before or after intraperitoneal infection with the highly reticulotropic Tulahuén strain of Trypanosoma cruzi produced enhanced resistance against the infection in mice. In contrast, C. parvum had no effect when the infection was caused with the predominately myotropic Y strain of T. cruzi. C. parvum given intravenously before immunization with killed culture forms of the Y strain parasite consistently diminished the protective effect against subsequent infection, which could be obtained with antigen alone.

Animals↗