Proteomic Mapping of Stimulus-Specific Signaling Pathways Involved in THP-1 Cells Exposed to Porphyromonas gingivalis or Its Purified Components

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• 作者：Julian A. Saba ; Mark E. McComb ; Donna L. Potts ; Catherine E. Costello ; Salomon Amar
• 刊名：Journal of Proteome Research
• 出版年：2007
• 出版时间：June 2007
• 年：2007
• 卷：6
• 期：6
• 页码：2211 - 2221
• 全文大小：741K
• 年卷期：v.6,no.6(June 2007)
• ISSN：1535-3907

文摘

Periodontitis is an inflammatory disease initiated by host-parasite interactions which contributes toconnective tissue destruction and alveolar bone resorption. Porphyromonas gingivalis (P.g.), a black-pigmented Gram-negative anaerobic bacterium, is a major pathogen in the development and progression of periodontitis. To characterize the role that P. gingivalis and its cell surface componentsplay in disease processes, we investigated the differential expression of proteins induced by live P.g.,P.g. LPS, and P.g. FimA, using two-dimensional gel electrophoresis in combination with massspectrometry. We have tested whether, at the level of protein expression, unique signaling pathwaysare differentially induced by the bacterial components P.g. LPS and P.g. FimA, as compared to live P.g.We found that P.g. LPS stimulation of THP-1 up-regulated the expression of a set of proteins comparedto control: deoxyribonuclease, actin, carbonic anhydrase 2, alpha enolase, adenylyl cyclase-associatedprotein (CAP1), protein disulfide isomerase (PDI), glucose regulated protein (grp78), and 70-kDa heatshock protein (HSP70), whereas FimA treatment did not result in statistically significant changes toprotein levels versus the control. Live P.g. stimulation resulted in 12 differentially expressed proteins:CAP1, tubulin beta-2 chain, ATP synthase beta chain, tubulin alpha-6 chain, PDI, vimentin, 60-kDa heatshock protein, and nucleolin were found to be up-regulated, while carbonic anhydrase II, beta-actin,and HSP70 were down-regulated relative to control. These differential changes by the bacteria and itscomponents are interpreted as preferential signal pathway activation in host immune/inflammatoryresponses to P.g. infection.