Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclear leukocyte apoptosis in vitro.
Porphyromonas gingivalis lipopolysaccharide delays human polymorphonuclear leukocyte apoptosis in vitro.
复制标题
牙龈卟啉单胞菌脂多糖在体外延迟人多形核白细胞凋亡。
DOI：
10.1111/j.1600-0765.1999.tb02242.x
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发表时间：
1999
影响因子：
3.5
通讯作者：
Walters,JD
中科院分区：
文献类型：
--
作者：
Preshaw,PM;Schifferle,RE;Walters,JD
Apoptosis (programmed cell death) is a mechanism by which superfluous or damaged cells undergo changes that lead to selective removal from organ systems by phagocytic cells. Certain bacterial products delay apoptosis in neutrophils (PMNs). In this study, PMNs were incubated for up to 8 h with varying concentrations of lipopolysaccharide (LPS), lipid A or capsular polysaccharide isolated from 3 strains ofPorphyromonas gingivalis (Pg)(strains HG‐184, A7A1‐28 and 381). Assay runs included controls containing cells and medium but no bacterial products. Fluorescence microscopy was used to evaluate apoptotic changes. PMNs exhibited a time‐dependent increase in the number of apoptotic cells. When cells were cultured in the presence of LPS from any of the 3Pgstrains, apoptosis was delayed in a dose‐dependent fashion (p <0.05). The effects of these LPS preparations were similar to each other and toEscherichia coli0111:B4 LPS. Lipid A from the 3Pgstrains also delayed apoptosis (p<0.05), but was less potent than LPS or synthetic lipid A. Capsular polysaccharide had no significant effect on apoptosis (p> 0.05). Thus, LPS and lipid A fromP. gingivalisappear to modulate the functional lifespan of PMNs. This could potentiate the inflammatory and destructive components of periodontal diseases.
