The cellular IgE response of rodents to infection with Nippostrongylus brasiliensis, Trichinella spiralis and Schistosoma mansoni

Abstract

The IgE response at the cellular level to helminthic infection was studied in BALB/c mice inoculated with the infective larvae of the nematodes Nippostronglylus brasiliensis (Nb) or Trichinella spiralis (Ts) or with the cercariae of the trematode Schistosoma mansoni (Sm). Changes in mesenteric lymph node (MLN) cell number, cell surface(s) IgD, IgM, IgE and Thy-1.2 and intracytoplasmic (c) IgE were recorded. In addition, a comparable study was conducted in rats infected with Nb. At 11 days after infection (DAI) of mice with Nb or Ts, or rats with Nb, there was a 3-fold increase in cell number in the MLN. There was a marked increase in cell number in the MLN of mice infected with Sm at 7 weeks after infection (WAI) and in the spleens of Sm-infected mice at 4 WAI. The percentage of cIgE + cells increased from undectectable levels in uninfected mice and rats to as high as 0.5–1.3% in the MLN of helminth-infected mice and rats. Analysis of cell surface molecules with a fluorescence activated cell sorter (FACS) showed that Nb and Ts infection induced slight increases in the percentages of B cells and slight decreases in the percentage of T cells. More remarkably, the percentage of sIgE + cells in the MLN of both Nb- and Ts-infected mice rose from undetectable levels in uninfected mice to 33 and 27%, respectively, at 15 DAI. This rise was stimulated in Ts-infected mice predominantly by adult Ts. In the MLN of Nb-infected rats, the percentage of cells that were sIgE + was greater than 50% at 15 DAI. However, there was no detectable increase in sIgE + cells in the spleen and MLN of Sm-infected mice until 5 WAI; peak levels of approximately 20% sIgE + cells were reached at 8 WAI. Treatment of MLN cells, from mice infected with Nb, Ts or Sm and rats infected with Nb, with pH 4.0 acetate buffer for 1 min (acid treatment) removed all detectable sIgE from greater than 90% of the sIgE + cells, but did not remove sIgD or sIgM from cells with these surface isotypes. The effect of acid treatment on sIgE was similar even after a secondary infection of mice or rats with nematode larvae. These data show that helminthic infection, in general, is a potent stimulator of the IgE system at the cellular level and that almost all of the sIgE + cells that arise have acquired cytophilic sIgE.