Premium
IMMUNOBLOTTING ANALYSIS OF HUMAN IgM, IgG AND IgA RESPONSE TO CHROMOSOMALLY CODED ANTIGENS OF YERSINIA ENTEROCOLITICA 0:3
Author(s) -
StåHlberg Tom H.,
Granfors Kaisa,
PekkolaHeino Kirsi,
Soppi Esa,
Toivanen Auli
Publication year - 1987
Publication title -
acta pathologica microbiologica scandinavica series c: immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0108-0202
DOI - 10.1111/j.1699-0463.1987.tb00011.x
Subject(s) - yersinia enterocolitica , antigen , yersinia , antibody , biology , epitope , serotype , immunology , yersinia infections , microbiology and biotechnology , enterobacteriaceae , bacteria , escherichia coli , genetics , gene
Human antibody response after Yersinia enterocolitica infection was studied by immunoblotting sequentially collected sera against a whole‐cell homogenate of Y. enterocolitica serotype 0:3, grown under conditions restrictive for the plasmid. The antibodies observed were directed against a multitude of chromosomally coded antigens, and a considerable individual heterogeneity was found in the reactions of individual sera. The early (0–2 months) and late (≥11 months) responses were directed against the same antigenic determinants. Antibodies against different bacterial epitopes decreased evenly with time, indicating that several, if not all, antigenic epitopes of the bacteria are responsible for the prolonged antibody production. IgM responses by most patients declined within a few months but were surprisingly strong in some even one year after onset of the infection. IgG antibodies showed a strong reaction against a region corresponding to lipid A and core of the bacterial LPS, whereas IgM and IgA recognized this region less often. No other significant differences between IgM, IgG and IgA responses were observed. Immunoblotting of sera from patients with post‐infection complications (arthritis, iritis, erythema nodosum) did not reveal any additional or specifically involved antigens. Altogether, these findings suggest that Yersiniae causing the original infection may hide in some of the patients for prolonged periods.