OBJECTIVE: To examine the role of lactoferrin (LF) on Toll like receptor 4 (TLR4) stimulated by lipopolysaccharide (LPS) in human periodontal ligament cells (hPDLCs). METHODS: Primary hPDLCs were cultured by tissue block enzymolytic method. Cells obtained from four passages were identified and used in this experiment. Cells without stimulation served as the controls and cells treated with LPS (0.1 microg x mL(-1)) comprised the LPS group. The LPS + LF group was pretreated with LPS (0.1 microg x mL(-1)) for 2 h, and then treated with LF (10 microg x mL(-1)). Four hours after LF stimulation, the mRNA expression levels of TLR4 were examined by real-time quantitative polymerase chain reaction (RT-PCR). The protein expression of TLR4 was observed by cell immunofluorescence staining after LF stimulation of 24 hours. RESULTS: TLR4 mRNA expression in the LPS + LF group was significantly more decreased than that in the LPS group (P < 0.05), but exhibited no difference with that in the control group (P > 0.05). Cell immunofluorescence staining showed that the protein expression of TLR4 in the LPS + LF group was significantly more decreased than that in the LPS group (P < 0.05), but exhibited no difference with that in the control group (P > 0.05). CONCLUSION: LF can decrease the expression of TLR4 stimulated by LPS in hPDLCs, thus presenting potential application for controlling the TLR4 immune pathway of periodontitis.
OBJECTIVE: To examine the role of lactoferrin (LF) on Toll like receptor 4 (TLR4) stimulated by lipopolysaccharide (LPS) in human periodontal ligament cells (hPDLCs). METHODS: Primary hPDLCs were cultured by tissue block enzymolytic method. Cells obtained from four passages were identified and used in this experiment. Cells without stimulation served as the controls and cells treated with LPS (0.1 microg x mL(-1)) comprised the LPS group. The LPS + LF group was pretreated with LPS (0.1 microg x mL(-1)) for 2 h, and then treated with LF (10 microg x mL(-1)). Four hours after LF stimulation, the mRNA expression levels of TLR4 were examined by real-time quantitative polymerase chain reaction (RT-PCR). The protein expression of TLR4 was observed by cell immunofluorescence staining after LF stimulation of 24 hours. RESULTS:TLR4 mRNA expression in the LPS + LF group was significantly more decreased than that in the LPS group (P < 0.05), but exhibited no difference with that in the control group (P > 0.05). Cell immunofluorescence staining showed that the protein expression of TLR4 in the LPS + LF group was significantly more decreased than that in the LPS group (P < 0.05), but exhibited no difference with that in the control group (P > 0.05). CONCLUSION: LF can decrease the expression of TLR4 stimulated by LPS in hPDLCs, thus presenting potential application for controlling the TLR4 immune pathway of periodontitis.