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Oral immunization of mice with Saccharomyces cerevisiae expressing a neutralizing epitope of Apx IIA exotoxin from Actinobacillus pleuropneumoniae induces systemic and mucosal immune responses
Author(s) -
Shin MinKyoung,
Lee WonJung,
Jung Myung Hwan,
Cha SeungBin,
Shin SeungWon,
Yoo Anna,
Kim DaeHyuk,
Yoo Han Sang
Publication year - 2013
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/1348-0421.12053
Subject(s) - biology , immune system , lamina propria , antigen , immunology , antibody , t cell , microbiology and biotechnology , epithelium , genetics
ABSTRACT An oral delivery system based on ApxIIA#5‐expressed on Saccharomyces cerevisiae was studied for its potential to induce immune responses in mice. Murine bone marrow‐derived dendritic cells (DCs) stimulated in vitro with ApxIIA#5‐expressed on S. cerevisiae upregulated the expression of maturation and activation markers, leading to production of tumor necrosis factor‐α, interleukin (IL)‐1β, IL‐12p70 and IL‐10. Presentation of these activated DCs to cluster of differentiation CD4+ T cells collected from mice that had been orally immunized with the ApxIIA#5‐expressed on S. cerevisiae elicited specific T‐cell proliferation. In addition, the orally immunized mice had stronger antigen‐specific serum IgG and IgA antibody responses and larger numbers of antigen‐specific IgG and IgA antibody‐secreting cells in their spleens, Peyer's patches and lamina propria than did those immunized with vector‐only S. cerevisiae or those not immunized. Furthermore, oral immunization induced T helper 1‐type immune responses mediated via increased serum concentrations of IgG2a and an increase predominantly of IFN‐γ‐producing cells in their spleens and lamina propria. Our findings suggest that surface‐displayed ApxIIA#5‐expressed on S. cerevisiae may be a promising candidate for an oral vaccine delivery system for eliciting systemic and mucosal immunity.