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Oral Infection augments the production of Inflammatory Markers of Atherogenesis.
Author(s) -
Meshkat Arash,
Hamidi Homa,
Mobayen Shirin,
Vakili Ladan,
Karimi Nika,
Navab Kaveh,
Kalantari Ryan,
Farazmand Maryam,
Haghnegahdar Maryam
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb497
Subject(s) - inflammation , gingivitis , medicine , systemic inflammation , immunology , oral infection , oral cavity , gastroenterology , dentistry
Objective To determine if oral infection will result in an increase in markers of inflammation that are known to augment atherogenesis. Introduction It is known that patients with inflammation or infection of the oral cavity have a higher risk of acquiring susceptibility and being in a state of systemic inflammation increasing their risk of having vascular abnormalities. In the present study we sought to examine if infection of the oral cavity would result in an increase in the levels of markers of atherogenesis. Methods Four month old female Apo E mice were treated with P. Gingivitis or with vehicle for 10 days. Plasma was prepared using heparinized capillary tubes and plasma separators and was cryopreserved. Circulating levels of interleukin 6 and 13‐HODE were determined using a commercially available ELISA kit and LC‐ESIMS/MS employing a Q4000 Quadrupole system. The data were analyzed using one way ANOVA taking advantage of GraphPad Prism application. Results In mice receiving the P. Gingivitis treatment the levels of circulating IL‐6 and 13‐HODE were significantly higher (p=0.011 and p=0.031, respectively). There was no difference in the levels of 20‐ HETE which is known not to increase in inflammation. Conclusion The present study indicates that oral infection with P. Gingivitis results in increases in the levels of circulating inflammatory molecules that are known to contribute to vascular dysfunction and increased vulnerability to atherogenic reactions.