Immunolocalization of lactoferrin in healthy and inflamed gingival tissues.

BACKGROUND: It has been reported that lactoferrin prevents biofilm formation and exerts antimicrobial activity. The aim of the present study was to evaluate the cellular source of lactoferrin in healthy and inflamed gingiva. METHODS: Lactoferrin synthesis was examined in relation to disease manifestation in biopsies of the marginal gingiva by immunohistochemistry. The expression of lactoferrin in cell cultures was studied by immunocytochemistry and reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: Healthy gingiva demonstrated no immunoreactivity to lactoferrin in epithelial and connective tissue cells. In inflamed specimens, lactoferrin staining was related to inflammatory cells. These results were confirmed by cell cultures of keratinocytes that did not show any immunoreactivity against lactoferrin. No mRNA message for lactoferrin was detected by RT-PCR in keratinocytes. CONCLUSIONS: These data provide evidence that lactoferrin is not synthesized in healthy gingival tissues. Therefore, elevated lactoferrin levels in the crevicular fluid of inflamed tissues originate from invading cells of the inflammatory reaction.

The novel human beta-defensin-3 is widely expressed in oral tissues.

The purpose of this study was to investigate the expression of human beta-defensins (hBD), especially of the recently discovered hBD-3, in oral tissues by reverse-transcription polymerase chain reaction (RT-PCR). Primary oral keratinocytes (n = 3) and fibroblasts (n = 3), 64 non-inflamed and 40 inflamed oral tissue samples, and 10 samples of salivary glands, were examined. The transcripts for hBD-3 (61/64), as well as for hBD-1 (64/64) and hBD-2 (54/64), were found to be widely expressed in non-inflamed oral tissues. In contrast, only 23, 22 and 24 of the 40 inflamed tissues showed detectable hBD-1, -2 and -3 transcripts, respectively. In salivary glands, mRNA expression was constitutive for hBD-1, frequent for hBD-2 (9/10), and infrequent for hBD-3 (4/10). Oral keratinocytes, but not fibroblasts, contained transcripts for all beta-defensins, suggesting that the novel hBD-3 is also produced in the epithelial compartment of oral tissues. The results indicate an important role for the novel hBD-3, as well as for hBD-1 and hBD-2, in the innate oral epithelial host defense.