title: Depressed autoantibody synthesis in Trypanosoma cruzi-infected rats born to mothers undergoing this infection during pregnancy.
abstract: Earlier work indicated that Trypanosoma cruzi infection in pregnant rats decreased the amount of myocardial damage that developed in their chronically infected offspring. Given the suspected role of autoimmune mechanisms in the generation of chronic myocarditis, we evaluated whether this maternal intervention was likely to affect the synthesis of autoantibodies in infected young. Autoantibodies were investigated against molecules exhibiting cross-reactivity with T. cruzi antigens or not, that is cerebroside sulphate (sulphatide) and actin, respectively. Female '1' rats (75 days old) that had been mated with syngeneic sires were separated into two groups, one challenged with living trypomastigotes at 7, 14 and 21 days following mating, and the other one given physiologic saline at the same intervals. At the time of weaning, offspring were injected with 10(6)/T. cruzi to constitute two infected groups: young born to infected mothers (InMoTc) and young delivered by uninfected mothers (CoMoTc). Serum antibodies were investigated by ELISA at 30 and 60 days post-infection, which represents acute and chronic infection, respectively. T. cruzi infection was associated with the production of anti-sulphatide antibodies, but the phenomenon was significantly less evident in InMoTc young and virtually unnoticeable during their chronic infection. Unlike the anti-sulphatide results, levels of anti-actin antibodies showed no differences between CoMoTc and InMoTc rats when compared during acute or chronic infection. The decreased production of anti-sulphatide autoantibodies of InMoTc offspring may be due to a modification of the immune repertoire of offspring because of the contact with parasite antigens during ontogeny.
authors.affiliation: Cátedra de Química Biologica, Facultad de Ciencias, Médicas de Rosario, Argentina.
authors.forename: S
authors.initials: S
authors.lastname: Feldman
authors.forename: S
authors.initials: S
authors.lastname: Revelli
authors.forename: H
authors.initials: H
authors.lastname: Davila
authors.forename: A
authors.initials: A
authors.lastname: Marcipar
authors.forename: M
authors.initials: M
authors.lastname: Rojas
authors.forename: J L
authors.initials: JL
authors.lastname: Avila
authors.forename: O A
authors.initials: OA
authors.lastname: Bottasso
mesh_terms: D000199:Actins / Q000276:immunology; D000818:Animals; D000953:Antigens, Protozoan; D001323:Autoantibodies / Q000096:biosynthesis*; D002598:Chagas Cardiomyopathy / Q000209:etiology / Q000276:immunology; D014355:Chagas Disease / Q000150:complications* / Q000276:immunology*; D005260:Female; D008297:Male; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D011247:Pregnancy; D015597:Pregnancy Complications, Parasitic / Q000276:immunology*; D051381:Rats; D013433:Sulfoglycosphingolipids / Q000276:immunology; D014349:Trypanosoma cruzi / Q000276:immunology
chemical_list: D000199:Actins; D000953:Antigens, Protozoan; D001323:Autoantibodies; D013433:Sulfoglycosphingolipids