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M Barral-Netto

Publications and source records attributed to M Barral-Netto.

82 records · Page 5Linked to original sources

Cell-mediated and humoral immune responses in capuchin monkeys infected with Schistosoma japonicum or Schistosoma mansoni.

Cell-mediated immune responses, assessed by lymphocyte clonal expansion in vitro, as well as humoral responses, assessed by an enzyme-linked immunosorbent assay (ELISA), were evaluated in capuchin monkeys during a 7-month infection with Schistosoma mansoni or with a Japanese or Philippine strain of Schistosoma japonicum. Although mounting a vigorous antibody response against parasite antigens, the S. mansoni-infected monkeys failed to show lymphocyte proliferation in response to stimulation with soluble adult worm antigen or soluble egg antigen derived from S. mansoni. Monkeys infected with S. japonicum responded to parasite antigens obtained from S. japonicum both by antibody production and lymphocyte blastogenesis. Monkeys infected with S. japonicum (Japanese strain) never developed detectable levels of circulating immune complexes (CIC). On the other hand high levels of CIC appeared at 7 months of infection in the monkeys infected with S. mansoni. The CIC levels exhibited negative correlations with intensity of infection. In studies of antigen species specificity, sera from S. mansoni-infected monkeys showed much higher IgG antibody titers to antigens derived from S. mansoni than to S. japonicum-derived antigens. On the other hand, monkeys infected with S. japonicum had comparable IgG antibody titers to antigens of both schistosome species.

Animals↗

Parasitological and pathological findings in capuchin monkeys infected with Schistosoma japonicum or Schistosoma mansoni.

Capuchin monkeys were studied for 7 months after exposure to Schistosoma mansoni or to either a Japanese or a Philippine strain of Schistosoma japonicum. The number of eggs present in the tissues and passed in the feces of S. mansoni-infected monkeys correlated well with the number of worm pairs recovered. Monkeys infected with the Philippine strain of S. japonicum passed large numbers of eggs in the feces and the number of these eggs correlated well with the number of worm pairs present. In monkeys infected with the Japanese strain of S. japonicum, fewer eggs were passed in the feces and there was little correlation with the number of worm pairs. Schistosome eggs were found predominantly in the small intestine in monkeys infected with the Philippine strain and predominantly in the colon in monkeys infected with the Japanese strain. The patterns of egg excretion in the feces and egg distribution in the tissues contrast with the patterns we recently described in rabbits, in which animals infected with the Philippine strain passed few eggs in the feces and showed a high proportion of tissue eggs in the colon. A single host species is thus shown to be inadequate to characterize the behavior of a schistosome strain.

Animals↗

Schistosoma mekongi infection in man: cellular immune responses and modulating mechanisms.

Cell-mediated immune responses (CMI), as assessed by lymphocyte proliferation in vitro, were evaluated in 11 Laotian patients harbouring asymptomatic chronic infections by Schistosoma mekongi, a schistosome closely related to S. japonicum. When the mononuclear cells of these patients were cultured in autologous plasma, lymphocyte responses to schistosome antigens were essentially nil, not differing from those of unexposed North American controls. Specific lymphocyte proliferation, however, was seen both after the removal of mononuclear cells that were nylon-wool-adherent and after substitution of the autologous serum in the culture with normal AB serum. Our data suggest that the CMI responses of humans with chronic S. mekongi infections are 'modulated' by adherent suppressor cells and serum-suppressive factors, and that modulation of CMI supports the stable host-parasite relationship in a similar fashion to that described for chronic human Schistosoma mansoni infection.

Adolescent↗

Characterizing subpopulations of neoplastic cells in serous effusions. The role of immunocytochemistry.

OBJECTIVE: To analyze the role of immunochemistry in serous effusions. STUDY DESIGN: We analyzed cell blocks of 18 pleural and 18 peritoneal effusions diagnosed as malignant (18), benign (14) and suspicious (4). They were immunostained by the avidin-biotin complex method with a panel of four monoclonal antibodies--CEA, Ber-EP4, LeuM1 (CD15) and p53--and, for lectins (Ulex europaeus) UEA-l, ConA and ConBr. RESULTS: Seventeen of the 18 cases of adenocarcinoma were positive for CEA (95%), 12 (66.6%) for Ber-EP4, 11 (61%) for CD15 and 11 (61%) for p53. Twelve of the 18 (66.6%) were positive for UEA-1, CEA, Ber-EP4 and CD15. UEA-1 did not react with mesothelial cells. p53 Gave a positive reaction in only one case, reactive mesothelial cells. ConA and ConBr reacted indiscriminately with benign and malignant cells; thus, it was not useful in distinguishing between these cells. CONCLUSION: In this context no antibody used alone is reliable for corroborating a diagnosis, but the selective use of a small panel of three markers (CEA, Ber-EP4 and LeuM1) can be very useful in solving diagnostic difficulties in the cytodiagnosis of serous effusions.

Adenocarcinoma↗

[Immunological aspects of infection of 6 inbred strains of mice by 3 different strains of Trypanosoma cruzi].

We evaluated humoral and cellular immune responses in 6 inbred mouse strains (BALB/c, B-10, C3H, A/J, AKR and DBA) infected with 3 Trypanosoma cruzi strains (Peruvian, 21 SF and Colombian), which are the standards for the 3 strains Types of Andrade's classification. Negative delayed-type hipersensitivity reactions to parasite antigens were evidence of suppressed cell-mediated immunity. An early drop of IgG1 and rise of IgM levels were observed in almost all mouse strains infected by any T. cruzi strain. Elevation of IgG2a and/or IgG2b levels was higher in resistant mouse strains. Anti-T. cruzi antibody levels (Indirect immunofluorescence and ELISA) did not correlate with survival. Despite some differences among mouse strains there was a definition of an overall pattern of host response and the maintenance of biological standards which characterize the basic types of T. cruzi strains.

Animals↗

Interleukin-2 production during murine infection by Leishmania mexicana amazonensis.

Highly susceptible BALB/c mice, resistant C57B1/6 and their F1 progeny (BDF1) were infected subcutaneously in the foot pad with Leishmania mexicana amazonensis. At various times after infection, spleen or draining popliteal lymph node cells were assayed for their capacity to generate Interleukin-2 (I1-2) by Concanavalin A (ConA) stimulation. In both BALB/c and C57B1/6 strains there was a transient increase in their capacity to produce I1-2, from the 3rd to the 10th week post-infection. Return to pre-infection levels occurred between 13th to 16th week post-infection in all three strains. BALB/c mice always produced higher titers of I1-2 than C57B1/6, but such differences were statistically significant only at 3 and 10 weeks post-infection. BDF1 mice had titers similar to those observed in BALB/c mice. I1-2 production by ConA-stimulated lymph node cells was lower as compared to the spleen, but with a similar pattern among the three mice strains. Our data show that susceptibility to infection by L. mexicana amazonensis is not associated with deficient ConA-stimulated I1-2 production.

Animals↗

A simple method for assessing the binding of concanavalin A to mononuclear cell surfaces: no interference of visceral leishmaniasis serum on this binding.

We report a simple method for evaluating the binding of concanavalin A (ConA) to human peripheral blood mononuclear cells (PBMC). The binding is evidenced by an immunoenzymic assay using peroxidase-conjugated immunoglobulins of a rabbit anti-ConA serum. Using the method we show that sera from patients with American leishmaniasis do not interfere with binding of ConA to PBMC.

Concanavalin A↗

A dhfr-ts- Leishmania major knockout mutant cross-protects against Leishmania amazonensis.

E10-5A3 is a dhfr-ts- Leishmania major double knockout auxotrophic shown previously to induce substantial protection against virulent L. major infection in both genetically susceptible and resistant mice. We investigated the capacity of dhfr-ts- to protect against heterologous infection by L. amazonensis. The degree of protection was evaluated by immunization of BALB/c or C57BL/6 mice with E10-5A3, followed by L. amazonensis challenge. Whether immunized by subcutaneous (SC) or intravenous (IV) inoculation, susceptible and resistant mice displayed a partial degree of protection against challenge with virulent L. amazonensis. SC-immunized BALB/c mice developed lesions 40 to 65% smaller than non immunized mice, while IV immunization led to protection ranging from 40 to 75% in four out of six experiments compared to non immunized animals. The resistant C57BL/6 mice displayed comparable degrees of protection, 57% by SC and 49% by IV immunization. Results are encouraging as it has been previously difficult to obtain protection by SC vaccination against Leishmania, the preferred route for human immunization.

Animals↗