Schistosomal granuloma modulation III. Schistosoma haematobium worms accelerate S-mansoni soluble egg antigen-induced hepatic granuloma formation in vivo

Recurrent experimental evidence indicates that schistosomal egg granuloma f ormation - at least in the murine model - results from a host response gene rated against both egg- and worm-derived antigens. Further experiments aime d at identifying the existence in vivo of cross-sensitization between Schis tosoma haematobium worms and S. mansoni-derived egg antigens were performed with respect to S. mansoni egg antigen-induced granuloma formation and fib rogenesis in the liver. Male OF1 mice bisexually infected with S. haematobi um or S. mansoni were hepatically challenged (cecal vein injection) with S. mansoni SEA (soluble egg antigen)-coupled Sepharose beads at the end of pr epatent infection (8-10 days prior to the start of egg deposition). The mea n granuloma volume (MGV) of in-vivo-generated synchronized hepatic granulom as (8 days old) and the fibrotic response were estimated. Just like S. mans oni-infected rodents, mice carrying an S. haematobium infection generated a n accelerated hepatic granulomogenesis [respective MGVs 4.72 +/- 0.56 and 5 .41 +/- 0.75 x 10(6) mu m(3); P < 0.0001 versus unsensitized (MGV 3.00 +/- 0.40 x 10(6) mu m(3)) mice] and an enhanced fibrotic response against S. ma nsoni SEA. They also had significantly enlarged spleens (P < 0.0001) and mo derately enlarged livers (P = 0.02) as compared with S. haematobium-infecte d mice that were not challenged with SEA. From these observations we infer that in vivo, S. haematobium worms can positively modulate S. mansoni egg a ntigen-induced granuloma formation and hepatic fibrogenesis, resulting in m ore severe liver pathology.