The Effect Of Periodontal Pathogen Pg-LPS On The Expression Of Inflammation And Apoptosis-Related Genes In Tissue-Specific Monocytes/Macrophages

Objective To provide a theoretical framework for understanding the relationshipbetween periodontal diseases and systemic disorders,this study investigated the effectof porphyromonas gingivalis lipopoly-sacchride on the inflammatory reaction (NO,ROS, NF-κB, IkBα) and apoptosis-related genes (caspase-3, Fas, p53, Bcl-2, Bax) indifferent parts of monocytes/macrophages from the same individual (normal/hyperlipemia rabbits). The effect of exogenous interlenkin-10has also been observed.Methods Monocytes/macrophages were isolated from different parts of the normaland hyperlipemia rabbits, including peripheral mononuclear cells, alveolar macro-phages, peritoneal macrophages and kupffer cells. The monocytes/macrophages werestimulated with porphyromonas gingivalis lipopolysacchride, Escherichia coliLipopolysacchride and interlenkin-10. NO levels were detected by Griess assay. ROSlevels were determined by Fluorescence enzyme-labelled meter with DCFH-DA asfluorescent probe. NF-κB p65and IκB-α fragment were detected by Western blot.Real Time-PCR was used to detect the mRNA expression of caspase-3, Fas, p53, Bcl-2and Bax.Results The different parts of monocytes/macrophages showed different expressionlevels of NO, ROS, NF-κB, IkBα. The expression level in hyperlipidemic rabbitswere higher than that in normal rabbits. Different parts of monocytes/macrophagesstimulated by1μg/ml Pg-LPS showed increased expression levels of NO, ROS, NF-κB, IkBα in the AM of normal rabbits and the Mo, AM, KC of hyperlipidemic rabbits;and inhibit the inflammatory reaction in the Mo of normal rabbits and the PM of hyperlipidemic rabbits. E.coli-LPS tended to show the same function as Pg-LPS withhigher stimulation. It was noted that0.1μg/ml IL-10could effectively inhibit theinflammatory reaction caused by the Pg-LPS. The expression of apoptosis-relatedgenes showed a different profile in different parts of monocytes/macrophages, however,the expression levels and the expression levels in hyperlipidemic rabbits were higherthan in normal rabbits. Hyperlipemia could induced the apoptosis of Mo, AM, PM andKC through the death receptor pathway. It was also found that1μg/ml Pg-LPSinduced the apoptosis of normal rabbit’s AM, KC and hyperlipidemic rabbit’s Mo,AM, PM and KC; but inhibited the apoptosis in the Mo, PM of normal rabbits.E.coli-LPS showed the same effect as Pg-LPS. We also noted that0.1μg/ml IL-10exertec no significant inhibitory effect on the apoptosis caused by the Pg-LPS.Conclusion The different parts of monocytes/macrophages showed differentexpression profile of inflammatory and apoptosis-related genes. The reaction ofinflammatory and apoptosis in hyperlipidemic rabbits was stronger than the normalrabbits. The Pg-LPS induced the different inflammatory reaction and apoptosis indifferent parts of monocytes/macrophages from the same individual (normal/hyperlipemia rabbits). KC in hyperlipidemia showedthe strongest inflammatoryreaction with the most effect catalytic effect for the apoptosis of PM. IL-10couldreduce the inflammatory reaction of Pg-LPS, but no significant effect on apoptosiswas observed.