Characteristics of Porphyromonas gingivalis lipopolysaccharide in co‐culture with Fusobacterium nucleatum. (24th January 2013)

• Record Type: Journal Article
• Authors: Lee, S.H.; Baek, D.H.
• Is Part Of: Molecular oral microbiology. Volume 28:Number 3(2013:Jun.)
• Page Start: 230
• Page End: 238
• Publication Date: 2013-01-24
• Subjects: Mouth -- Microbiology -- Periodicals; Respiratory infections -- Microbiology -- Periodicals; Mouth -- Diseases -- Immunological aspects -- Periodicals; 617.522
• DOI: 10.1111/omi.12020
• Languages: English
• ISSNs: 2041-1006

Abstract

<abstract abstract-type="main" id="omi12020-abs-0001"> <title>Summary</title> <p> <italic>Porphyromonas gingivalis</italic> is associated with chronic periodontitis and forms multi‐species biofilms. They can communicate within species as well as with other species found in the subgingiva, which may induce changes in the growth ratio and virulence of periodontopathogens. The lipopolysaccharide (LPS) of <italic>P. gingivalis</italic> shows different virulence by growth condition. The purpose of this study was to investigate the characteristics of <italic>P. gingivalis </italic>LPS when co‐cultured with <italic>Fusobacterium nucleatum</italic>. After culture of <italic>P. gingivalis</italic> in the presence or absence of <italic>F. nucleatum</italic>, <italic> P. gingivalis </italic>LPS was extracted. THP‐1 cells were treated with the LPS and induction of cytokine expression was investigated using real‐time reverse transcription polymerase chain reaction (RT‐PCR) and enzyme‐linked immunosorbent assay (ELISA). For the analysis of <italic>P. gingivalis </italic>LPS, LPS biosynthesis‐related genes such as <italic>lpxA</italic> and <italic>lpxD</italic> were evaluated with real‐time RT‐PCR. Finally, molecular mass of lipid A was measured by mass spectrometry after hydrolysis of the LPS. Co‐cultured <italic>P. gingivalis </italic>LPS exhibited higher induction of expression of interleukin 1β, 6, and 8 than single‐cultured <italic>P. gingivalis </italic>LPS. These symptoms may be caused by an increase in <italic>m</italic>/<italic>z</italic> 1689 lipid A through the upregulation of <italic>lpxA</italic> and <italic>lpxD</italic> expression by communication between <italic>P. gingivalis</italic> and <italic>F. nucleatum</italic>.</p> </abstract>