Congenital and nursing effects on the evolution of Schistosoma mansoni infection in mice

Abstract

Modification of the immune response to schistosomal infection in children or offspring born to mother R infected with Schistosoma mansoni has been demonstrated in human and in experimental schistosomiasis. One of the hypothesis to explain this fact could be the transfer of circulating antigens and antibodies from mother to foetus through the placenta or from mother to child by milk. The results of this spontaneous transference are controversial in the literature. In an attempt to investigate these questions, we studied one hundred and twenty offspring (Swiss mice), sixty born to infected-mothers (group A) and sixty born to non-infected mothers (group B). These were percutaneously infected with 50 cercariae/mouse, and divided in six sub-groups (20 mice/sub-group), according to the following schedule: after birth (sub-groups A.I and B.I), 10 days old (sub-groups A.II and B.II) and 21 days old (sub-groups A.III and B.III). After the exposure period, the young mice returned to their own mothers for nursing. Six weeks later, the mice were killed. We obtained the following results: 1) There is transference of antibody to cercariae (CAP), adult worms (SWAP) and egg antigens (SEA) from the infected mothers to the offspring, probably through placenta and milk; 2) Offspring born to infected mothers exhibit much less coagulative hepatic necrosis and show a lower number of eggs in the small intestine and a less intense and predominant exsudative stage of the hepatic granulomas when compared with the exsudative-productive stage of the control groups. The findings suggest that congenital and nursing factors can interfere on the development of the schistosomiasis infection, causing an hyporesponse to the eggs.

Susceptibility of neonate mice born to Schistosoma mansoni-infected and noninfected mothers to subsequent S. mansoni infection

“…b Liver egg granuloma in mice born to infected mothers (infected group). c No granuloma was detected in four mice born to S. mansoni-infected mothers 1970; Lenzi et al 1987). The present findings suggest that the maternal transfer of S. mansoni Abs and/or Ags to fetus and their persistence in offspring up to 8 weeks after delivery may have induced immunologic tolerance, which modified susceptibility of these mice against S. mansoni challenge.…”

“…It is also known that Ags responsible for the hyopresponsiveness in the offspring apparently emanate from the eggs (Hang et al 1974), which react with the lymphoid cells of the immune system during their developing in the prenatal period and in some way specifically suppress any future response of these cells to that Ags when they reach immunological activity (Roitt 1988). Lenzi et al (1987) showed that hyopresponsiveness to infection with apparent best protection is observed in offspring of infected mothers especially after nursing period (after 21 days), and that could be due to transfer of Abs and Ags via placenta and/or milk. The precise mechanism by which how in utero exposure of fetal immune system to parasite Ags leads to Ag-specific hyporesponsiveness is still not clear.…”

Influence of maternal schistosomiasis on the immunity of adult offspring mice

“…Exposure to S. mansoni prenatally and during breastfeeding modulates the immunity against the homologous antigen in postnatal infection, which leads to a reduction in the size and quantity of egg granuloma in the offspring's liver (Hang et al 1974;Lenzi et al 1987;Attallah et al 2006). These findings were associated with a fetal/neonatal sensibilization through the transference of circulating schistosomal antigens and maternal parasite-specific antibodies by way of the placenta and breast milk (Lenzi et al 1987;Attallah et al 2003).…”

“…As described above, the hyporesponsiveness to homologous schistosomal antigen in the offspring has been attributed to previous antigen contact and immunity factors acquired from the infected mothers, as there are anti-S. mansoni antibodies and a regulatory environment in pregnancy (Lenzi et al 1987;Attallah et al 2006). However, the effects of S. mansoni maternal infection on the immune responses to a heterologous antigen in the adult offspring are poorly defined.…”

Maternal Helminth Infections

“…Murine studies revealed transfer of antibodies to cercariae (CAP), adult worms (SWAP), and egg antigens (SEA) from infected mothers to the offspring probably through placenta and breastmilk indicating the possibility of prenatal immune priming. Indeed, offspring born to infected mothers exhibited much less coagulative hepatic necrosis and showed a lower number of eggs in the small intestine and a less intense and predominant exsudative stage of the hepatic granulomas upon infection [112]. These findings suggest that exposure to S. mansoni during breastfeeding modulates the immunity against the homologous antigen in postnatal infection towards protection of the host.…”