Porphyromonas gingivalis lipopolysaccharide alters atherosclerotic-related gene expression in oxidized low-density-lipoprotein-induced macrophages and foam cells

Abstract

P. gingivalis LPS appears to be an important factor in the development of atherosclerosis by stimulation of atherosclerosis-related gene expression in both macrophages and foam cells via activation of the NF-κB pathway.

Silencing Triggering Receptors Expressed on Myeloid Cells-1 Impaired the Inflammatory Response to Oxidized Low-Density Lipoprotein in Macrophages

“…The slides were washed with propanol and then rinsed with PBS. Finally, the cells were treated with hematoxylin for 1 min to stain nuclei [1]. To quantify intracellular lipid contents in oxLDL treated macrophages, Oil Red was extracted by 100 % isopropanol (10 min on a shaker) before hematoxylin counter staining and the absorbance was read at 510 nm with a microplate reader [15].…”

“…The LDL fraction was oxidized by a 12-h treatment with CuSO4, as described previously [1]. Oxidative modification of LDL was assessed by measuring thiobarbituric acid-reactive substances as previously described [14].…”

“…Moreover, TREM-1 has complex signal integration with certain TLRs [9]; in particular, it was observed that TREM-1 is an amplifier of TLR-induced inflammatory response upon bacterial invasion [10]. Most studies have focused on determining the involvement of TREMs in the inflammatory processes induced by microorganisms or specific TLR agonist [1,[10][11][12]. However, whether the biologically active oxLDL can trigger TREMs and its potential effect in atherosclerotic lesion onset and progression has not been investigated.…”

“…Atherosclerosis is a chronic progressive inflammatory disease characterized by the accumulation of lipid and fibrous elements in arterial walls, which is driven by responses of both innate and adaptive immunity [1,2]. Many studies have demonstrated that oxidized low-density lipoprotein (oxLDL) contributes to the development of atherosclerosis, a process in which macrophages play a central role through the induction of the inflammatory response and foam cell formation [3,4].…”

Human β-defensin-3 alleviates the progression of atherosclerosis accelerated by Porphyromonas gingivalis lipopolysaccharide

“…In addition, many studies demonstrate that P. gingivalis LPS promotes macrophages transformation to foam cells. The expression of pro-inflammatory cytokines, growth factors, and adhesion molecules in macrophages is upregulated by P. gingivalis LPS [12][13][14][15][16]. Collectively, these findings indicate that P. gingivalis LPS from periodontal lesions may contribute to the development of AS.…”