Table 2.

Hepatic alterations in wild-type and IL-9-expressing transgenic mice with received acute or chronicS. mansoni infectionsa

Infection and groupGranuloma diam (μm)Fibrosis (μg of collagen/mg)EosinophiliabMastocytosiscHepatocyte damaged (AST SFU/ml)
Granuloma (%)No. of eosinophils (107/g)
Acute
 Wild-type305 ± 208.5 ± 1.947 ± 11NDe ND349 ± 64
 Transgenic311 ± 449.1 ± 2.651 ± 9ND ND360 ± 59
Chronic
 Wild-type274 ± 2314.1 ± 3.434 ± 1821.6 ± 4.53.4 ± 2.3245 ± 28
 Transgenic250 ± 3512.3 ± 2.564 ± 27f 41.3 ± 11.7f 9.1 ± 3.4f 210 ± 37
  • a Hepatic alterations in wild-type mice and transgenic mice that constitutively expressed IL-9. Both sets of mice were exposed to acute (150-cercaria) or chronic (25-cercaria)S. mansoni infections. Data are from eight acutely and five chronically infected mice that were killed on days 56 and 72 after infection, respectively. Data are presented as means ± standard deviations and are representative of two separate experiments.

  • b Hepatic eosinophilia is presented as a percentage of eosinophils within the granuloma and as the number of eosinophils per gram of protein.

  • c Mastocytosis was determined by measurement of mMCP-1 activity in liver homogenates and is presented as milligram of protease activity per gram of protein.

  • d Hepatocyte damage was quantified by assay for plasma aspartate aminotransferase (AST) activity.

  • e ND, not determined.

  • f Significantly greater in transgenic mice than in wild-type mice (P < 0.01 by Student's ttest).