Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human PMN gene expression and enhance bactericidal capacity

被引:41
|
作者
Graves, Shawna F. [1 ,3 ]
Kobayashi, Scott D. [1 ]
Braughton, Kevin R. [1 ]
Whitney, Adeline R. [1 ]
Sturdevant, Daniel E. [2 ]
Rasmussen, Devon L. [1 ]
Kirpotina, Liliya N. [4 ]
Quinn, Mark T. [4 ]
DeLeo, Frank R. [1 ]
机构
[1] NIAID, Lab Bacterial Pathogenesis, NIH, Hamilton, MT USA
[2] NIAID, Genom Unit, Res Technol Branch, Rocky Mt Labs,NIH, Hamilton, MT 59840 USA
[3] Univ Montana, Div Biol Sci, Dept Biochem & Biophys, Missoula, MT 59812 USA
[4] Montana State Univ, Dept Immunol & Infect Dis, Bozeman, MT 59717 USA
基金
美国国家卫生研究院;
关键词
MRSA; priming; neutrophil; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; TUMOR-NECROSIS-FACTOR; HUMAN-NEUTROPHILS; RECEPTOR (TLR)2; UNITED-STATES; GM-CSF; ACTIVATION; LIPOPOLYSACCHARIDE; BINDING; PHAGOCYTOSIS;
D O I
10.1189/jlb.1111575
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
CA-MRSA infections are often caused by strains encoding PVL, which can cause lysis of PMNs and other myeloid cells in vitro, a function considered widely as the primary means by which PVL might contribute to disease. However, at sublytic concentrations, PVL can function as a PMN agonist. To better understand this phenomenon, we investigated the ability of PVL to alter human PMN function. PMNs exposed to PVL had enhanced capacity to produce O-2 (-) in response to fMLF, but unlike priming by LPS, this response did not require TLR signal transduction. On the other hand, there was subcellular redistribution of NADPH oxidase components in PMNs following exposure of these cells to PVL-a finding consistent with priming. Importantly, PMNs primed with PVL had an enhanced ability to bind/ ingest and kill Staphylococcus aureus. Priming of PMNs with other agonists, such as IL-8 or GM-CSF, altered the ability of PVL to cause formation of pores in the plasma membranes of these cells. Microarray analysis revealed significant changes in the human PMN transcriptome following exposure to PVL, including up-regulation of molecules that regulate the inflammatory re- sponse. Consistent with the microarray data, mediators of the inflammatory response were released from PMNs after stimulation with PVL. We conclude that exposure of human PMNs to sublytic concentrations of PVL elicits a proinflammatory response that is regulated in part at the level of gene expression. We propose that PVL-mediated priming of PMNs enhances the host innate immune response. J. Leukoc. Biol. 92: 361-374; 2012.
引用
收藏
页码:361 / 374
页数:14
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