期刊
JOURNAL OF PERIODONTOLOGY
卷 73, 期 6, 页码 624-630出版社
AMER ACAD PERIODONTOLOGY
DOI: 10.1902/jop.2002.73.6.624
关键词
iron binding; saliva/analysis; Actinobacillus actinomycetemcomitans; periodontitis/drug therapy; lactoferrin/therapeutic use
资金
- NIDCR NIH HHS [DE10592] Funding Source: Medline
Background: Actinobacillus actinomycetemcomitans (Aa) is associated with localized aggressive periodontal disease in juveniles (LAgP). Lactoferrin (LF) is an iron-binding salivary protein that has been shown to kill Aa in its iron-free form (apo) and reduce binding to host cells in its iron-saturated form (halo). However, recent in vitro studies show that LF does not kill clinical isolates of Aa, and LF with reduced levels of bound iron does not interfere with its attachment. These findings suggest that colonization of Aa may occur more readily in an environment containing LF with low iron levels. The purpose of this study was to examine the relationship of LF iron levels in saliva of LAgP patients as compared to their age-, gender-, and race-matched controls. Methods: Whole and parotid saliva was collected from LAgP patients and matched controls. Micrograms of LF/mg of protein as well as nanograms of iron/mug of L.F were determined. Iron binding was determined in parotid saliva by addition of nonlabeled and Fe-59 labeled iron. Results: LAgP patients' whole saliva had higher LF levels than controls, but their LF contained less iron (P less than or equal to0.005). No iron was found in LF from parotid saliva in either group. When iron was added to parotid saliva, the LAgP saliva bound 20 to 30 times less iron than controls (P less than or equal to0.001). Finally, LF was identified as the major iron-binding protein in parotid saliva by Fe-59 autoradiography and Western blotting. Conclusions: This study shows that the level of bound iron in LF is significantly reduced in LAgP patients compared to controls. These data suggest that LF from LAgP patients has a reduced capacity to bind iron and that LF iron levels may play an important role in Aa-induced LAgP.
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