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The Journal of Immunology, 1999, 162: 3559-3565.
Copyright © 1999 by The American Association of Immunologists

Nasopharyngeal-Associated Lymphoreticular Tissue (NALT) Immunity: Fimbriae-Specific Th1 and Th2 Cell-Regulated IgA Responses for the Inhibition of Bacterial Attachment to Epithelial Cells and Subsequent Inflammatory Cytokine Production1

Manabu Yanagita*,{dagger}, Takachika Hiroi*, Noriko Kitagaki*, Shigeyuki Hamada{ddagger}, Hiro-o Ito§, Hidetoshi Shimauchi{dagger}, Shinya Murakami{dagger}, Hiroshi Okada{dagger} and Hiroshi Kiyono2,*

* Department of Mucosal Immunology, Research Institute for Microbial Diseases, and Departments of {dagger} Periodontology and Endodontology, and {ddagger} Oral Microbiology, Faculty of Dentistry, Osaka University, Osaka, Japan; and § Department of Preventive Dentistry, Kagoshima University Dental School, Kagoshima, Japan

To investigate the antibacterial activity of mucosal Th1 and Th2 immune responses induced nasally and orally, mice were immunized with mucosal vaccine containing fimbrial protein of Porphyromonas gingivalis, a causative agent for a destructive chronic inflammation in the periodontium, and cholera toxin (CT) as mucosal adjuvant. Nasal vaccine containing low doses of fimbriae (10 µg) and CT (1 µg) induced Ag-specific Th1/Th2-type response in CD4+ T cells in mucosal effector tissues, including nasal passage and submandibular glands, which accounted for the generation of Ag-specific IgA-producing cells. In contrast, oral immunization required higher amounts of fimbriae and CT for the induction of Ag-specific IgA responses. Fimbriae-specific IgA mAbs generated from submandibular glands of nasally immunized mice inhibited P. gingivalis attachment to and reduced subsequent inflammatory cytokine production from epithelial cells. These findings suggest that nasal vaccination is an effective immunization regimen for the induction of Ag-specific Th1 and Th2 cell-driven IgA immune responses that possess the ability to inhibit bacterial attachment to epithelial cells and subsequent inflammatory cytokine production.




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