Open AccessSublingual vaccination with fusion protein consisting of the functional domain of hemagglutinin A of P orphyromonas gingivalis and E scherichia coli maltose‐binding protein elicits protective immunity in the oral cavity
Author(s) -
Yuzawa Satoshi,
KuritaOchiai Tomoko,
Hashizume Tomomi,
Kobayashi Ryoki,
Abiko Yoshimitsu,
Yamamoto Masafumi
Publication year - 2012
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2011.00895.x
Subject(s) - porphyromonas gingivalis , maltose binding protein , antigen , immunology , fusion protein , biology , immunization , microbiology and biotechnology , antibody , immunoglobulin g , immune system , medicine , recombinant dna , periodontitis , biochemistry , gene
This study demonstrated that sublingual immunization with a fusion protein, 25k‐hag A ‐ MBP , which consists of a 25‐ kD a antigenic region of hemagglutinin A purified from P orphyromonas gingivalis fused to maltose‐binding protein ( MBP ) originating from E scherichia coli as an adjuvant, elicited protective immune responses. Immunization with 25k‐hag A ‐ MBP induced high levels of antigen‐specific serum IgG and IgA , as well as salivary IgA . High level titers of serum IgG and IgA were also induced for almost 1 year. In an IgG subclass analysis, sublingual immunization with 25k‐hag A ‐ MBP induced both IgG 1 and IgG 2b antibody responses. Additionally, numerous antigen‐specific IgA antibody‐forming cells were detected from the salivary gland 7 days after the final immunization. Mononuclear cells isolated from submandibular lymph nodes ( SML s) showed significant levels of proliferation upon restimulation with 25k‐hag A ‐ MBP . An analysis of cytokine responses showed that antigen‐specific mononuclear cells isolated from SML s produced significantly high levels of IL ‐4, IFN ‐γ, and TGF ‐β. These results indicate that sublingual immunization with 25k‐hag A ‐ MBP induces efficient protective immunity against P . gingivalis infection in the oral cavity via T h1‐type and T h2‐type cytokine production.