Effects of anti-IgE mAb on serum IgE, FcεRII/CD23 expression on splenic B cells and worm burden in mice infected with <i>Paragonimus westermani</i>

, Shin, M H; , Min, H K

doi:1997.35.1.47

Korean J Parasito > Volume 35(1):1997 > Article

Original Article


Korean J Parasitol. 1997 Mar;35(1):47-54. English. Published online Mar 20, 1997. http://dx.doi.org/10.3347/kjp.1997.35.1.47
Copyright © 1997 by The Korean Society for Parasitology


Effects of anti-IgE mAb on serum IgE, FcεRII/CD23 expression on splenic B cells and worm burden in mice infected with Paragonimus westermani
M H Shin,^* and H K Min
Department of Parasitology, College of Medicine, Ewha Womans University, Seoul 158-056, Korea.


Abstract
It is generally accepted that parasite-specific IgE plays a crucial role in host defense against helminthic parasites. However, the role of high levels of nonspecific IgE in helminthic infections is still controversial. To investigate the role of nonspecific IgE in primary infections with P. westermani, the effect of anti-IgE mAb treatment on serum IgE, FcεRII/CD23 expression and worm burden in Paragonimus-infected mice were examined. In mice treated with anti-IgE antibody, the total IgE levels were not detectable (1 µg/ml) throughout the experiment compared with untreated infected mice. The mean percentages of FcεRII/CD23 positive splenic B cells in anti-IgE treated mice (range: 20.3 - 30.5) were also decreased throughout the experiment compared with untreated infected mice (range: 35.7 - 44.4). Reduction of the total IgE and expression of FcεRII/CD23 on splenic B cells resulted in decreased worm burden six weeks post infection. These results suggest that high levels of nonspecific IgE in mice with primary infections of P. westermani play a harmful, rather than beneficial, role for the host, perhaps by interfering with CD23-dependent cellular pathways.

Figures


	Fig. 1 Effect of anti-IgE mAb on total serum IgE levels in BALB/c mice infected with P. westermani. Total serum IgE levels were determined by ELISA using monoclonal rat anti-mouse IgE.


	Fig. 2 Effect of anti-IgE mAb in parasite-specific IgE levels in BALB/c mice infected with P. westermani. Absorbance (O.D) was measured at 450 mn. Asterisk (*) denotes significant difference (P<0.05) between infected mice treated with PBS and infected mice treated with anti-IgE mAb.


	Fig. 3 Suppressive effect of anti-IgE on the expression of FcεRII/CD23 on splenic B cell in mice infected with P. westermani. FL1-H and FL2-H indicate green fluorescence (CD23) and red fluorescence (CD45R/B220). respectively. Results ard shown as two color contour plots (A, autofluorescence; B, non-infected mice; C, infected mice treated with PFB; D, infected mice treated with anti-IgE mAb).

Tables


	Table 1 Effect of anti-IgE in the precent (%) of FcεRII/CD23 positive splenic B cells in mice infected with Paragonimus westermani


	Table 2 Effect of anti-IgE on the number of worms recovered in mice infected with Paragonimus westermani

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