Biomedical subjects

J Leiro

Publications and source records attributed to J Leiro.

57 records · Page 4Linked to original sources

PubMed1987

The antiphosphorylcholine plaque-forming cell responses induced by the nematode Trichinella in BWF1 mice.

We have tested the ability of the nematode Trichinella to infect young and old (NZB x NZW) F1 (BWF1) mice. We report the capacity of these mice to respond to the parasite antigens containing the epitope phosphorylcholine. The values obtained in adult worm intestinal retention rates and in the number of encysted larvae on the 35th day postinfection showed that the old BWF1 mice are more susceptible than young BWF1 and control (BALB/c x CBA/j)F1 (BCF1) mice to Trichinella infection. However, unlike the BCF1 mice, young BWF1 mice were unable to produce a good anti-phosphorylcholine plaque-forming cell response after the killing of Trichinella larvae by the anthelminthic mebendazole. Old BWF1 mice presented a discrete response which is discussed. Finally, our results seem to indicate that the lack of anti-phosphorylcholine response in young BWF1 mice after mebendazole treatment may be related to the high susceptibility of these mice to the suppressive properties of encysted Trichinella larvae against their own antigens.

Age Factors↗

PubMed1987

Immune response to Trichinella epitopes: the antiphosphorylcholine plaque-forming cell response during the biological cycle.

Phosphorylcholine (PC), an immunodominant component of the cell wall of certain bacteria, fungi and nematodes, is known to induce low anti-PC antibody levels during natural infection by Trichinella spiralis. This article reports a study in which spleen cells from BCF1 mice infected with Trichinella sp. larvae were found to produce large numbers of direct haemolytic plaques in response to PC conjugated to sheep red blood cells (SRBC) after muscle-encysted larvae had been killed by treatment with mebendazole. Inhibition of the response by PC-chloride, immunodiffusion and immunoelectrophoretic studies with the anti-PC IgA (TEPC-15) and anti-idiotype T15 serum assays showed the plaque-forming cell (PFC) response to be specific for PC. The absence of haemolytic plaques when unconjugated SRBC or TNP-SRBC were used as indicator cells ruled out involvement of a polyclonal response. Greatest anti-PC PFC response was found to be associated with a microsomal fraction designated FCp1, a particulate fraction behaving as a thymus-dependent antigen. The FCp1 fractions from all four strains of Trichinella employed induced anti-PC PFC responses when injected into mice. These results suggest that FCp1 is a suitable antigen for use in detailed studies of immune responses to Trichinella and related parasites.

Animals↗

PubMed1987

Modulation of the anti-phosphorylcholine immune response during Trichinella spiralis infections in mice.

The nematode Trichinella spiralis is able to modulate the antibody response, as measured by the plaque-forming cell (PFC) technique, to three thymus-dependent (TD) antigens: (1) a heterologous antigen unrelated to the parasite (sheep red blood cells (SRBC]; (2) an antigenic fraction, rich in phosphorylcholine (PC), obtained from T. spiralis (FCp1) and (3) a heterologous antigen unrelated to the parasite, but sharing the PC epitope with the FCp1 fraction (PC-KLH). During the life-cycle of the parasite in BCF1 mice, two opposing immunomodulating activities occur: (1) an immuno-potentiating activity in mice infected during the intestinal and larval migratory stages, for all three antigens, and (2) a carrier-specific immunosuppressive response in mice infected and immunized with the FCp1 fraction during the muscle phase of the life-cycle. The anti-PC PFC response of these mice is dependent on the infection dose and decreases from day 35 post-infection (p.i.) until at least day 85 p.i. The factor responsible for the stimulating effect observed during this stage is the presence of migratory larvae in the host. All the foregoing seems to indicate that T. spiralis can use specific suppression mechanisms to aid in its own survival.

Animals↗