Authors: Bengtsson, T.¹; Karlsson, H.²; Gunnarsson, P.¹; Skoglund, C.¹; Elison, C.²; Leanderson, P.²; Lindahl, M.²

Source: Journal of Internal Medicine, Volume 263, Number 5, May 2008 , pp. 558-571(14)

Publisher: Wiley-Blackwell

Abstract:

.  Bengtsson T, Karlsson H, Gunnarsson P, Skoglund C, Elison C, Leanderson P, Lindahl M (Linköping University, Linköping, Sweden). The periodontal pathogen Porphyromonas gingivalis cleaves apoB-100 and increases the expression of apoM in LDL in whole blood leading to cell proliferation. J Intern Med 2008; 263: 558-571. Objective. 

Several studies support an association between periodontal disease and atherosclerosis with a crucial role for the pathogen Porphyromonas gingivalis. This study aims at investigating the proteolytic and oxidative activity of P. gingivalis on LDL in a whole blood system using a proteomic approach and analysing the effects of P. gingivalis-modified LDL on cell proliferation. Methods. 

The cellular effects of P. gingivalis in human whole blood were assessed using lumi-aggregometry analysing reactive oxygen species production and aggregation. Blood was incubated for 30 min with P. gingivalis, whereafter LDL was isolated and a proteomic approach was applied to examine protein expression. LDL-oxidation was determined by analysing the formation of protein carbonyls. The effects of P. gingivalis-modified LDL on fibroblast proliferation were studied using the MTS assay. Results. 

Incubation of whole blood with P. gingivalis caused an extensive aggregation and ROS production, indicating platelet and leucocyte activation. LDL prepared from bacteria-exposed blood showed an increased protein oxidation, elevated levels of apoM and formation of two apoB-100 N-terminal fragments. Porphyromonas gingivalis-modified LDL markedly increased the growth of fibroblasts. Inhibition of gingipain R suppressed the modification of LDL by P. gingivalis. Conclusions. 

The ability of P. gingivalis to change the protein expression and proliferative capacity of LDL may represent a crucial event in periodontitis-associated atherosclerosis.

Keywords: atherosclerosis; growth factors; infection; inflammation; lipoproteins

Document Type: Original article

DOI: http://dx.doi.org/10.1111/j.1365-2796.2007.01917.x

Affiliations: 1: From the Division of Pharmacology, Department of Medical and Health Sciences, Faculty of Health Sciences, Cardiovascular Inflammation Research Centre, Linköping University, Linköping 2: Division of Occupational and Environmental Medicine, Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Cardiovascular Inflammation Research Centre, Linköping University, Linköping; Sweden

Publication date: 2008-05-01

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