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Biomedical subjects

H O Davila

Publications and source records attributed to H O Davila.

5 recordsLinked to original sources
PubMed2000

Protected Trypanosoma cruzi infection in rats born to mothers receiving interferon-gamma during gestation is associated with a decreased intramacrophage parasite growth and preferential synthesis of specific IgG2b antibodies.

We demonstrated that administration of interferon gamma (IFN-gamma) to pregnant rats conferred partial resistance in their offspring to further challenge with Trypanosoma cruzi. Because of the effects of IFN-gamma on macrophage activation and immunoglobulin isotype selection, offspring were now studied to ascertain whether this intervention modifies the in vitro replication of T. cruzi and nitric oxide (NO) production by peritoneal macrophages (PE), together with the anti-T. cruzi IgG isotypes. To evaluate the possibility of a detrimental effect of IFN-gamma, serum levels of anti-sulphatide autoantibodies were also investigated. Offspring were born to mothers undergoing one of the following procedures during gestation: treatment with recombinant rat IFN-gamma, 50,000 IU/rat, five times/week for 3 weeks, which was started on the day of mating; infection with 10(6) trypomastigotes of T. cruzi at 7, 14, and 21 days after mating plus IFN-gamma treatment as given to the former group; the same protocol except that physiological saline was injected instead of IFN-gamma; injection of physiological saline only. Offspring were challenged at weaning with a similar dose of T. cruzi, to constitute four groups of infected young, plus an additional group of age-matched uninfected rats born to control mothers. PE were harvested at day 7 postinfection (pi), exposed to parasites and further investigated for the replication of T. cruzi and NO production, whereas ELISA studies for measuring serum anti-T. cruzi IgG subclasses and anti-sulphatide autoantibodies were performed at day 30 pi. The number of intracellular parasites in PE was markedly decreased in young born to IFN-gamma-treated mothers, this not being accompanied by higher nitrite levels in culture supernatants. Offspring delivered by IFN-gamma-treated mothers showed no higher serum concentrations of anti-sulphatide autoantibodies, but exhibited a preferential synthesis of anti-T. cruzi IgG2b antibodies. This rat isotype is known to fix complement and constitutes the rat counterpart of IgG2a mouse immunoglobulins whose synthesis is favoured by IFN-gamma.

Animals↗
PubMed1996

Protection of young rats from acute Trypanosoma cruzi infection by interferon-gamma given to their mothers during pregnancy.

We investigated whether administration of interferon-gamma (IFN-gamma) to pregnant rats, infected or not with Trypanosoma cruzi, was likely to protect their offspring from trypanosomal infection. Upon mating with syngeneic sires, four groups of 70-day-old female 1 rats were subjected to one of the following procedures: treatment with recombinant rat (Rr)IFN-gamma 50,000 IU/rat five times/week for three weeks; infection with 1 x 10(6) trypomastigotes of T. cruzi at 7, 14, and 21 days after mating plus IFN-gamma treatment as given to the former group; the same protocol but IFN-gamma injections being replaced by injection with physiologic saline. Offspring were nursed by their mothers until weaning and then infected with a similar dose of T. cruzi. Pregnant rats showed no exacerbated infection but a self-resolving mild disease, regardless of whether or not they had received IFN-gamma. Maternal infection with T. cruzi and/or IFN-gamma treatment did not affect gestational outcome. Offspring born to both groups of IFN-gamma-treated mothers were almost fully protected from acute infection, and showed higher levels of anti-T. cruzi IgG antibodies when compared with young born to their respective IFN-gamma-untreated mothers. Measurements of IFN-gamma serum activities indicated that ameliorated acute disease in offspring whose mothers were given IFN-gamma during gestation, was not associated with increased levels of endogenously produced IFN-gamma.

Animals↗
PubMed1994

Infection with Trypanosoma cruzi during pregnancy in rats and a decrease in chronic myocardial lesions in their infected offspring.

To ascertain whether maternal infection with Trypanosoma cruzi may influence the course of the parasitic infection in offspring, two groups of female 1 rats were mated with syngeneic sires. One group of females was infected with 10(6) trypomastigotes of T. cruzi three times at weekly intervals. All offspring were nursed by their mothers until weaning and then separated into two groups of young, one to be infected with the same dose of T. cruzi, and the other to remain uninfected. Infection of pregnant rats caused no aggravated disease but resulted in a self-controlled infection that did not cause any deaths or affect their reproductive capacity. The number of young delivered, litter size, fertility coefficient, and offspring weights at weaning were also unaffected by maternal infection; however, the survival coefficient decreased in comparison with values recorded in the offspring of uninfected mothers. The latter finding is likely due to neonatal transmission, since bloodstream forms of T. cruzi were observed in a few offspring of infected mothers. While infected offspring whose mothers had been inoculated with T. cruzi during pregnancy were not protected from acute infection, the occurrence of chronic focal myocarditis was less prevalent when compared with that recorded in chronically infected offspring born to uninfected mothers.

Acute Disease↗
PubMed1990

Depressed adjuvant arthritis in rats transferred with spleen cells from Trypanosoma cruzi-infected syngeneic donors.

In the present study we investigated whether the attenuating effect of chronic Trypanosoma cruzi (Tc) infection on adjuvant arthritis (AA) in the rat could be transferred to naive recipients. Transfer of whole spleen cells, but not of serum, from Tc-infected rats reduced AA (means +/- SEM: 11 +/- 0.5) in recipient animals (control values, means +/- SEM: 19 +/- 0.7). Transfer of a T-cell-enriched subpopulation from spleen cells of Tc-infected rats (obtained by filtration through a nylon wool column) resulted in a similar attenuation of AA (means +/- SEM: 7.5 +/- 2.2). The arthritic response of rats intraperitoneally inoculated with 2 x 10(5) Tc 48 h before induction did not differ from that observed in controls. Neither parasites nor specific antibodies were observed in suckling mice inoculated with serum or cell suspensions employed in transfer experiments. Consequently, the depressive effect on AA could not be directly attributed to Tc per se. We hypothesize that a homeostatic immunosuppressor mechanism may be responsible for this phenomenon.

Animals↗