Porphyromonas gingivalis Lipopolysaccharide Induced Proliferation and Activation of Natural Killer Cells in Vivo.

Yuhua Wang,Li Xu,Jun-O Jin,Wei Zhang

doi:10.3390/molecules21081086

Abstract

Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS) promoted different innate immune activation than that promoted by Escherichia coli (E. coli) LPS. In this study, we examined the effect of P. gingivalis LPS on the proliferation and activation of natural killer (NK) cells in vivo and compared that function with that of E. coli LPS. Administration of P. gingivalis LPS to C57BL/6 mice induced stronger proliferation of NK cells in the spleen and submandibular lymph nodes (sLNs) and increased the number of circulating NK cells in blood compared to those treated with E. coli LPS. However, P. gingivalis LPS did not induce interferon-gamma (IFN-γ) production and CD69 expression in the spleen and sLN NK cells in vivo, and this was attributed to the minimal activation of the spleen and sLN dendritic cells (DCs), including low levels of co-stimulatory molecule expression and pro-inflammatory cytokine production. Furthermore, P. gingivalis LPS-treated NK cells showed less cytotoxic activity against Yac-1 target cells than E. coli LPS-treated NK cells. Hence, these data demonstrated that P. gingivalis LPS promoted limited activation of spleen and sLN NK cells in vivo, and this may play a role in the chronic inflammatory state observed in periodontal disease.

Highlights

Porphyromonas gingivalis (P. gingivalis) is a gram-negative anaerobic bacterium implicated as one of the major pathogens contributing to the development of chronic inflammatory periodontal diseases [1]
C57BL/6 mice were treated intravenously (i.v.) with 1 mg/kg of P. gingivalis LPS or E. coli LPS for 18 h [28,29] Treatment with P. gingivalis LPS induced significant decreases in the number and frequency of CD3− NK1.1+ cells in the spleen and submandibular lymph nodes (sLNs) compared to null-treatment controls (Figure 1A,B), whereas the number of CD3+ NK1.1− cells were not changed by P. gingivalis LPS (Figure 1A,B)
In contrast to the spleen and sLN natural killer (NK) cells, the number of blood NK cells were significantly increased by P. gingivalis LPS (Figure 1A lower panels and B right panels)

Summary

Introduction

Porphyromonas gingivalis (P. gingivalis) is a gram-negative anaerobic bacterium implicated as one of the major pathogens contributing to the development of chronic inflammatory periodontal diseases [1]. Lipopolysaccharide (LPS) in the surface components of P. gingivalis interacts with the innate immune cell-expressed toll-like receptors (TLRs), which provokes the release of chemokines and cytokines [2,3,4]. Cells, macrophages, and dendritic cells (DCs)—accelerates inflammatory responses, which contributes to the clearance of the invading pathogens [5]. Previous studies have shown that P. gingivalis LPS promotes a different innate immune activation compared to that of Escherichia coli (E. coli) LPS [3,6]. Systemic administration of E. coli LPS induces a potent stimulus for tumor necrosis factor-alpha (TNF-α) production in the mouse, whereas P. gingivalis LPS has a minimal stimulatory capacity on TNF-α production [7]. P. gingivalis LPS activates macrophages weakly compared to E. coli

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Conclusion