The impact of Staphylococcus aureus-associated molecular patterns on staphylococcal superantigen-induced toxic shock syndrome and pneumonia.
The impact of Staphylococcus aureus-associated molecular patterns on staphylococcal superantigen-induced toxic shock syndrome and pneumonia.
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DOI：
10.1155/2014/468285
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发表时间：
2014
影响因子：
4.6
通讯作者：
Rajagopalan G
中科院分区：
文献类型：
--
作者：
Tilahun AY;Karau M;Ballard A;Gunaratna MP;Thapa A;David CS;Patel R;Rajagopalan G
金黄色葡萄球菌能够引起一系列人类疾病。在严重的S。金黄色葡萄球菌感染，葡萄球菌病原体相关分子模式（PAMP），如肽聚糖，脂磷壁酸，脂蛋白，甚至完整的S。金黄色葡萄球菌，被认为与葡萄球菌超抗原（SSAg）联合作用，分别激活先天性和适应性免疫系统，并引起免疫病理学。然而，最近的研究表明，葡萄球菌PAMPs可以通过多种机制抑制炎症，并保护免受葡萄球菌中毒性休克综合征，一种由致炎性链球菌引起的危及生命的全身性疾病。金黄色。考虑到葡萄球菌PAMPs的促炎和抗炎作用的矛盾，我们研究了S。使用HLA-DR 3和HLA-DQ 8转基因小鼠，研究了金黄色葡萄球菌衍生的分子模式对SSAg体内驱动的免疫应答的影响。我们的研究表明，S.金黄色葡萄球菌衍生的肽聚糖（PGN）、脂磷壁酸（LTA）和热灭活的金黄色葡萄球菌（HKSA）在体外抑制SSAg诱导的T细胞增殖。它们不能拮抗SSAg在体内的免疫刺激作用，如通过它们不能减弱全身性细胞因子/趋化因子应答和减少SSAg诱导的T细胞扩增所确定的。这些葡萄球菌PAMP也不能保护HLA-DR 3和HLA-DQ 8转基因小鼠免受SSAg诱导的中毒性休克或由产生SSAg的S.金黄色。
Staphylococcus aureus is capable of causing a spectrum of human illnesses. During serious S. aureus infections, the staphylococcal pathogen-associated molecular patterns (PAMPs) such as peptidoglycan, lipoteichoic acid, and lipoproteins and even intact S. aureus, are believed to act in conjunction with the staphylococcal superantigens (SSAg) to activate the innate and adaptive immune system, respectively, and cause immunopathology. However, recent studies have shown that staphylococcal PAMPs could suppress inflammation by several mechanisms and protect from staphylococcal toxic shock syndrome, a life-threatening systemic disease caused by toxigenic S. aureus. Given the contradictory pro- and anti-inflammatory roles of staphylococcal PAMPs, we examined the effects of S. aureus-derived molecular patterns on immune responses driven by SSAg in vivo using HLA-DR3 and HLA-DQ8 transgenic mice. Our study showed that neither S. aureus-derived peptidoglycans (PGN), lipoteichoic acid (LTA), nor heat-killed Staphylococcus aureus (HKSA) inhibited SSAg-induced T cell proliferation in vitro. They failed to antagonize the immunostimulatory effects of SSAg in vivo as determined by their inability to attenuate systemic cytokine/chemokine response and reduce SSAg-induced T cell expansion. These staphylococcal PAMPs also failed to protect HLA-DR3 as well as HLA-DQ8 transgenic mice from either SSAg-induced toxic shock or pneumonia induced by a SSAg-producing strain of S. aureus.
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影响因子：
32.4
作者：
Reynolds JM;Pappu BP;Peng J;Martinez GJ;Zhang Y;Chung Y;Ma L;Yang XO;Nurieva RI;Tian Q;Dong C
通讯作者：
Dong C
影响因子：
5.4
作者：
Mangalam, Ashutosh;Rodriguez, Moses;David, Chella
通讯作者：
David, Chella
影响因子：
32.4
作者：
Khare S;Dorfleutner A;Bryan NB;Yun C;Radian AD;de Almeida L;Rojanasakul Y;Stehlik C
通讯作者：
Stehlik C
影响因子：
4.6
作者：
Rajagopalan, Govindarajan;Tilahun, Ashenafi Y.;David, Chella S.
通讯作者：
David, Chella S.
影响因子：
120.7
作者：
Klevens, R. Monina;Morrison, Melissa A.;Fridkin, Scott K.
通讯作者：
Fridkin, Scott K.