The Effect of Toll-like Receptor 2 Activation on the Non-opsonic Phagocytosis of Oral Bacteria and Concomitant Production of Reactive Oxygen Species by Human Neutrophils
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- 2016.05.03
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서지정보
ㆍ발행기관 : 대한구강생물학회
ㆍ수록지정보 : International Journal of Oral Biology / 41권 / 1호
ㆍ저자명 : Kap Youl Kim, Youngnim Choi
목차
Introduction
Materials and Methods
Results
Discussion
Acknowledgements
Conflict of interest
References
영어 초록
Chronic/cyclic neutropenia, leukocyte adhesion deficiency syndrome, Papillon-Lefèvre syndrome, and Chédiak-Higashi syndrome are associated with severe periodontitis, suggesting the importance of neutrophils in the maintenance of periodontal health. Various Toll-like receptor (TLR) ligands are known to stimulate neutrophil function, including FcR-mediated phagocytosis. In the present study, the effect of TLR2 activation on the non-opsonic phagocytosis of oral bacteria and concomitant production of reactive oxygen species (ROS) by human neutrophils was evaluated. Neutrophils isolated from peripheral blood were incubated with Streptococcus sanguinis or Porphyromonas gingivalis in the presence of various concentrations of Pam3CSK4, a synthetic TLR2 ligand, and analyzed for phagocytosis and ROS production by flow cytometry and chemiluminescence, respectively. Pam3CSK4 significantly increased the phagocytosis of both bacterial species in a dose-dependent manner. However, the enhancing effect was greater for S. sanguinis than for P. gingivalis. Pam3CSK4 alone induced ROS production in neutrophils and also increased concomitant ROS production induced by bacteria. Interestingly, incubation with P. gingivalis and Pam3CSK4 decreased the amounts of ROS, as compared to Pam3CSK4 alone, indicating the possibility that P. gingivalis survives within neutrophils. However, neutrophils efficiently killed phagocytosed bacteria of both species despite the absence of Pam3CSK4. Although P. gingivalis is poorly phagocytosed even by the TLR2-activated neutrophils, TLR2 activation of neutrophils may help to reduce the colonization of P. gingivalis by efficiently eliminating S. sanguinis , an early colonizer, in subgingival biofilm.
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