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Lack of immunological cross-reactivity between parasite-derived and recombinant forms of ES-62, a secreted protein of Acanthocheilonema viteae

Published online by Cambridge University Press:  11 October 2005

C. A. EGAN
Affiliation:
Department of Immunology, University of Strathclyde, Glasgow G4 0NR, UK
K. M. HOUSTON
Affiliation:
Department of Immunology, University of Strathclyde, Glasgow G4 0NR, UK
M. J. C. ALCOCER
Affiliation:
Division of Nutritional Sciences, University of Nottingham, Loughborough LE12 5RD, UK
A. SOLOVYOVA
Affiliation:
Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow G12 8QQ, UK
R. TATE
Affiliation:
Department of Physiology and Pharmacology, University of Strathclyde, Glasgow G4 0NR, UK
G. LOCHNIT
Affiliation:
Institute of Biochemistry, University of Giessen, Giessen D35392, Germany
I. B. McINNES
Affiliation:
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow G11 6NT, UK
M. M. HARNETT
Affiliation:
Division of Immunology, Infection and Inflammation, University of Glasgow, Glasgow G11 6NT, UK
R. GEYER
Affiliation:
Institute of Biochemistry, University of Giessen, Giessen D35392, Germany
O. BYRON
Affiliation:
Division of Infection and Immunity, Institute of Biomedical and Life Sciences, University of Glasgow G12 8QQ, UK
W. HARNETT
Affiliation:
Department of Immunology, University of Strathclyde, Glasgow G4 0NR, UK
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Abstract

The longevity of filarial nematodes is dependent on secreted immunomodulatory products. Previous investigation of one such product, ES-62, has suggested a critical role for post-translationally attached phosphorylcholine (PC) moieties. In order to further investigate this, ES-62 lacking PC was produced, using the Pichia pastoris recombinant gene expression system. Unlike parasite-derived ES-62, which is tetrameric the recombinant material was found to consist of a mixture of apparently stable tetramers, dimers and monomers. Nevertheless, the recombinant protein was considered to be an adequate PC-free ES-62 as it was recognized by existing antisera against the parasite-derived protein. However, subsequent to this, recognition of parasite-derived ES-62 by antibodies produced against the recombinant protein was found to be absent. In an attempt to explain this, recombinant ES-62 was subjected to structural analysis and was found to (i) contain 3 changes in amino acid composition; (ii) demonstrate significant alterations in glycosylation; (iii) show major differences in protein secondary structure. The effects of these alterations in relation to the observed change in immunogenicity were investigated and are discussed. The data presented clearly show that recognition by existing antibodies is insufficient proof that recombinant proteins can be used to mimic parasite-derived material in studies on nematode immunology and vaccination.

Information

Type
Research Article
Copyright
2005 Cambridge University Press
Figure 0

Fig. 1. (A) PAGE of parasite-derived and recombinant ES-62: 2·5 μg of parasite-derived (lane 1), and recombinant ES-62 (lane 2) with ovalbumin (lane 3) as a control were run on 12% polyacrylamide gels under non-reducing, non-denaturing conditions. The gels were fixed and stained with Sigma Brilliant Blue Colloidal-G Stain. The solid arrows indicate ES-62 (lane 1), rES-62 (Lane 2) and ovalbumin. (B) SDS-PAGE/Western blotting of parasite-derived and recombinant ES-62 with polyclonal rabbit anti-ES-62 serum: 2·5 μg of parasite-derived (lane 1), and recombinant ES-62 (lane 2) with ovalbumin (lane 3) as a control were run on 12% polyacrylamide gels under reducing, denaturing conditions. The polypeptides were transferred to a nitrocellulose membrane and then probed with a polyclonal rabbit anti-ES-62 serum followed by an anti-rabbit horseradish peroxidase-conjugated secondary antibody. Molecular weight markers (kDa) are indicated on the left of the gels. (C) Dot-blot analysis of parasite-derived and recombinant ES-62 with a monoclonal anti-ES-62 antibody: 1·25 μg of parasite-derived (lane 1), and recombinant ES-62 (lane 2) with ovalbumin as a control (lane 3) were placed on nitrocellulose Hybond-C (Amersham) and analysed by dot blot using a monoclonal anti-ES-62 antibody directed against a conformational epitope on the parasite-derived ES-62 tetramer. (D) SDS-PAGE of parasite-derived and recombinant ES-62 with TEPC15: 2·5 μg of parasite-derived (lane 1), and recombinant ES-62 (lane 2) with ovalbumin (lane 3) as a control were run on 12% polyacrylamide gels under reducing, denaturing conditions, transferred to a nitrocellulose membrane, then probed with TEPC15 followed by an anti-mouse Ig horseradish peroxidase-conjugated secondary antibody. Molecular weight markers (kDa) are indicated on the left of the gel.

Figure 1

Fig. 2. (A) Recognition of recombinant ES-62 by IgG1 antibodies in serum of mice inoculated with recombinant or parasite-derived ES-62. Groups of 5 Balb/C mice were injected weekly with 2 μg parasite-derived (squares) or recombinant (triangles) ES-62 and serum samples taken. Samples were analysed by ELISA for recombinant ES-62 specific IgG1 responses in duplicate and mean values calculated±standard error of the mean. Results are expressed as reciprocal end-point dilution. (B) Recognition of parasite-derived ES-62 by IgG1 antibodies in serum of mice inoculated with parasite-derived or recombinant ES-62. Groups of 5 Balb/C mice were injected weekly with 2 μg parasite-derived (squares) or recombinant (triangles) ES-62 and serum samples taken. Samples were analysed by ELISA for parasite-derived ES-62 specific IgG1 responses in duplicate and mean values calculated±standard error of the mean. Results are expressed as reciprocal end-point dilution. (C) Recognition of denatured parasite-derived ES-62 by IgG1 antibodies in serum of mice inoculated with parasite-derived ES-62. Groups of 5 Balb/C mice were injected weekly with 2 μg parasite-derived ES-62 and serum samples taken. Samples were analysed by ELISA for denatured (filled squares) and non-denatured (open squares) parasite-derived ES-62 specific IgG1 responses in duplicate and mean values calculated±standard error of the mean. Results are expressed as reciprocal end-point dilution. (D) Recognition of denatured recombinant ES-62 by IgG1 antibodies in serum of mice inoculated with recombinant ES-62. Groups of 5 Balb/C mice were injected weekly with 2 μg recombinant ES-62 and serum samples taken. Samples were analysed by ELISA for denatured (filled triangles) and non-denatured (open triangles) recombinant ES-62 specific IgG1 responses in duplicate and mean values calculated±standard error of the mean. Results are expressed as reciprocal end-point dilution.

Figure 2

Fig. 3. Circular dichroism and sedimentation velocity characterization of rES-62. (A) Far UV circular dichroism spectrum for rES-62 (solid line) and parasite-derived ES-62 (dashed line) in phosphate buffer (91·5 mM Na2HPO4, 58·5 mM NaH2PO4, pH 7·4). The spectra were normalized for concentration. (B) Size distribution c(s); interference data obtained for monomeric loading concentrations of 165 μM (solid line) 123 μM (dashed line) 82 μM (dotted line) 41 μM (dashed-dotted line) 12 μM (short dashed line) 10 μM (dashed-dotted-dotted line). (C) The concentration dependence of s: ‘monomer’ (squares), ‘dimer’ (circles), ‘tetramer’ (triangles). The horizontal solid line marks the sedimentation coefficient obtained experimentally for parasite-derived ES-62 (Ackerman et al. 2003); dotted lines are the linear extrapolation of s20,w to zero concentration for the 3 species.

Figure 3

Table 1. Sedimentation coefficients for ES-62 extrapolated to zero concentration and corrected to standard conditions

Figure 4

Fig. 4. (A) PAGE of recombinant ES-62 and N-type glycosylation site knock-out rES-62 mutants: 2·5 μg of parasite-derived ES-62 (lane 1), recombinant ES-62 (lane 2), N-type glycosylation site 1 (a.a. 194) knock-out (lane 3), N-type glycosylation site 2 (a.a. 235) knock-out (lane 4), N-type glycosylation site 3 (a.a. 325) knock-out (lane 5), were run on 12 % polyacrylamide gels under non-reducing, non-denaturing conditions. The gels were fixed and stained with Sigma Brilliant Blue Colloidal-G Stain. (B) Recognition of recombinant ES-62 lacking N-type glycosylation sites by IgG1 antibodies in serum of mice inoculated with parasite-derived or recombinant ES-62. Groups of 5 Balb/c mice were injected weekly with 2 μg parasite-derived or recombinant ES-62 and serum samples taken. Samples were analysed by ELISA for each of 3 distinct N-type glycosylation site knock-out rES-62 mutant recognition by IgG1 antibodies in duplicate and mean values calculated±standard error of the mean. Results are expressed as reciprocal end-point dilutions.

Figure 5

Fig. 5. (A) PAGE of recombinant ES-62 (I) and recombinant ES-62 (II): 2·5 μg of parasite-derived (lane 1), recombinant ES-62 (I) (lane 2), and recombinant ES-62 (II) (lane 3) were run on 12 % polyacrylamide gels under non-reducing, non-denaturing conditions. The gels were fixed and stained with Sigma Brilliant Blue Colloidal-G Stain. (B) Recognition of recombinant ES-62 (II) by IgG1 antibodies in serum of mice inoculated with parasite-derived or recombinant ES-62. Groups of 5 Balb/c mice were injected weekly with 2 μg parasite-derived or recombinant ES-62 (I) and serum samples taken. Samples were analysed by ELISA for rES-62 (II) specific IgG1 responses in duplicate and mean values calculated±standard error of the mean. Results are shown as reciprocal end-point dilutions.