Journal
INTERNATIONAL JOURNAL FOR PARASITOLOGY
Volume 35, Issue 9, Pages 1023-1030Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ijpara.2005.03.019
Keywords
roundworm; Ascaris suum; recombinant As24; protective response; moulting inhibition
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Previous studies have shown that antigens from various life-cycle stages of Ascaris suum can induce host-protective immunity against challenge infections with infective eggs of A. suum. This study evaluated whether Escherichia coli-expressed recombinant 24-kDa antigen from A. suum (rAs24) was a suitable vaccine candidate for the control of Ascaris infections by examining its performance in a mouse model. Immunization of BALB/c mice in three consecutive doses with rAs24 in Freund's Complete Adjuvant (FCA) results in protection against challenge infections as manifested by a 58% reduction (P < 0.001) in recovery and stunted development of A. suum lung-stage larvae at day 7 post-challenge. Sera obtained from immune protected mice had a significantly increased level of immunoglobulin G (IgG) (P < 0.0001) but had no IgE response. Analysis of IgG-subclass profiles revealed that IgG1 (P < 0.0001) showed the greatest increase followed by IgG2b (P < 0.005), IgG2a (P < 0.006) and IgG3 (P < 0.04). Splenic T cells from rAs24-FCA immunized mice secreted significantly high levels of both Th1 cytokine gamma-interferon (P < 0.005) and Th2 cytokine interleukin-10 (P < 0.001) after stimulation with rAs24 in vitro. Interestingly, affinity purified anti-rAs24 IgG was shown to inhibit moulting of A. suum lung-stage L3 to L4 in vitro by 26%, indicating an in vivo function of the endogenous As24 in the moulting processes. An intense expression of endogenous As24 in the hypodermis and gut epithelium of A. suum lung-stage L3 by immunofluorescence supports a function for endogenous As24. These findings may contribute to the understanding of rAs24-induced Th1/Th2-mediated effector mechanisms required for the protection of A. suum lung-stage larval infection. (c) 2005 Australian Society for Parasitology Inc. Published by Elsevier Ltd. All rights reserved.
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