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Title: DEFENSIN-INDUCED ADAPTIVE IMMUNITY IN MICE AND ITS POTENTIAL IN PREVENTING PERIODONTAL DISEASE

Author
item Brogden, Kim
item Heidari, Mohammad
item Sacco, Randy
item Palmquist, Debra
item GUTHMILLER, J - UNIVERSITY OF IOWA
item JOHNSON, G - UNIVERSITY OF IOWA
item JIA, H - UNIVERSITY OF IOWA
item TACK, B - UNIVERSITY OF IOWA
item MCCRAY, P - UNIVERSITY OF IOWA

Submitted to: Oral Microbiology and Immunology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/17/2003
Publication Date: 4/1/2003
Citation: Brogden, K.A., Heidari, M., Sacco, R.E., Palmquist, D.E., Guthmiller, J.M., Johnson, G.K., Jia, H.P., Tack, B.F., Mccray, P.B. 2003. Defensin-induced adaptive immunity in mice and its potential in preventing periodontal disease. Oral Microbiology and Immunology. Vol. 18:95-99.

Interpretive Summary: Defensins are known to have antimicrobial activity. Recently, however, they have been shown to play other roles in host defense. For example, they have the ability to alter the adaptive immune response. In the present study, we show that defensins induce unique immune responses when co-administered with a protein antigen. The results suggest that it may be possible to modify the host immune response to vaccines by co-administration of specific defensins. It might therefore be possible to skew the immune response in a desirable direction.

Technical Abstract: The severity of periodontal disease is dependent on a combination of host, microbial agent and environmental factors. One strong correlate related to periodontal disease pathogenesis is the immune status of the host. Here we show that human neutrophil peptide (HNP) defensins or human beta-defensins (HBD), co-administered intranasally with the antigen ovalbumin (OVA), induce unique immune responses that if used with microbial antigens may have the potential to hinder the pathogenesis of periodontal disease. C57BL/6 mice were immunized intranasally with phosphate buffered saline (PBS) containing 1 microgram HNP-1, HNP-2, HBD1 or HBD2 with and without 50 micrograms OVA. At 21 days, isotypes and subclasses of OVA-specific antibodies were determined in saliva, serum, nasal wash, bronchoalveolar lavage fluid, and fecal extracts. OVA-stimulated splenic lymphoid cell cultures from immunized mice were assessed for interferon (IFN)-gamma, Interleukin (IL)-4 and IL-10. In comparison with mice immunized with only OVA, HNP-1 and HBD2 induced significantly higher (P<0.05) OVA-specific serum IgG, lower, but not significant, serum IgM and significantly lower (P<0.05) IFN-gamma. In contrast, HNP-2 induced low OVA-specific serum IgG and higher, but not significant, serum IgM. HBD1 induced significantly higher (P<0.05) OVA-specific serum IgG, higher, but not significant, serum IgM, and significantly higher (P<0.05) IL-10. The elevated serum IgG subclasses contained IgG1 and IgG2b.