Immunogenicity and protection against Glaesserella parasuis serotype 13 infection after vaccination with recombinant protein LolA in mice
Glaesserella parasuis is a pathogen causing Glässer’s disease characterized by fibrinous polyserositis, polyarthritis, and meningitis. Owing to the low cross-immunogenicity of different bacterial antigens in commercial vaccines, finding and identifying effective immunoprotective antigens will facili...
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Published in | Journal of Veterinary Medical Science Vol. 84; no. 11; pp. 1527 - 1535 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Japan
JAPANESE SOCIETY OF VETERINARY SCIENCE
2022
Japan Science and Technology Agency The Japanese Society of Veterinary Science |
Subjects | |
Online Access | Get full text |
ISSN | 0916-7250 1347-7439 1347-7439 |
DOI | 10.1292/jvms.22-0203 |
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Summary: | Glaesserella parasuis is a pathogen causing Glässer’s disease characterized by fibrinous polyserositis, polyarthritis, and meningitis. Owing to the low cross-immunogenicity of different bacterial antigens in commercial vaccines, finding and identifying effective immunoprotective antigens will facilitate the development of novel subunit vaccines. In this study, LolA, identified by bioinformatics approaches, was cloned and successfully expressed as a recombinant protein in Escherichia coli, and its immunogenicity and protection were evaluated in a mouse model. The results showed that the recombinant protein LolA can stimulate mice to produce high levels of IgG antibodies and confer 50% protection against challenge with the highly virulent G. parasuis CY1201 strain (serotype 13). By testing the cytokine levels of interleukin 4 (IL-4), IL-10, and interferon-γ (IFN-γ), it was found that the recombinant protein LolA can induce both Th1 and Th2 immune responses in mice. These results suggest that the recombinant protein LolA has the potential to serve as an alternative antigen for a novel vaccine to prevent G. parasuis infection. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 These authors contributed equally to this work. |
ISSN: | 0916-7250 1347-7439 1347-7439 |
DOI: | 10.1292/jvms.22-0203 |