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 micro g
HNP-1,
HNP-2, HBD1 or HBD2 with and without 50 microg 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.