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在不同抗生素存在下培养的表皮葡萄球菌的上清液可诱导人单核细胞中肿瘤坏死因子α的不同释放。

Supernatants from Staphylococcus epidermidis grown in the presence of different antibiotics induce differential release of tumor necrosis factor alpha from human monocytes.

作者信息

Mattsson E, Van Dijk H, Verhoef J, Norrby R, Rollof J

机构信息

Eijkman-Winkler Institute for Medical Microbiology, Infectious Diseases, and Inflammation, Utrecht, The Netherlands.

出版信息

Infect Immun. 1996 Oct;64(10):4351-5. doi: 10.1128/iai.64.10.4351-4355.1996.

DOI:10.1128/iai.64.10.4351-4355.1996
PMID:8926110
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC174378/
Abstract

Bacterial products from gram-positive bacteria, such as peptidoglycan, teichoic acid, and toxins, activate mononuclear cells to produce tumor necrosis factor alpha (TNF). The present study evaluated the release of soluble cell wall components from Staphylococcus epidermidis capable of inducing TNF after exposure of the bacteria to various antibiotics. A clinical S. epidermidis isolate (694) was incubated with either penicillin, oxacillin, vancomycin, or clindamycin at five times the MIC. Supernatants of the cultures obtained by filtration were added to plastic adherent monocytes in the absence or presence of human serum. After 18 h of incubation, monocyte supernatants were tested for the presence of TNF by enzyme-linked immunosorbent assay (ELISA). Supernatants from bacteria incubated with beta-lactam antibiotics induced higher TNF levels than those obtained from bacteria incubated with culture medium only (no antibiotics), vancomycin, or clindamycin. Human serum potentiated supernatant-induced TNF release, especially in beta-lactam supernatants. The soluble peptidoglycan and teichoic acid contents of supernatants, as estimated by inhibition ELISA and, for peptidoglycan, also by affinity depletion with vancomycin-Sepharose gel, were proportional to TNF release. Differences in the ability of individual antibiotics to generate TNF-releasing products from S. epidermidis were observed, the most potent antibiotics being penicillin and oxacillin.

摘要

革兰氏阳性菌产生的细菌产物,如肽聚糖、磷壁酸和毒素,可激活单核细胞产生肿瘤坏死因子α(TNF)。本研究评估了表皮葡萄球菌在接触各种抗生素后能够诱导TNF产生的可溶性细胞壁成分的释放情况。将一株临床分离的表皮葡萄球菌(694)与青霉素、苯唑西林、万古霉素或克林霉素以五倍最低抑菌浓度(MIC)进行孵育。通过过滤获得的培养物上清液在有无人血清的情况下加入塑料贴壁单核细胞中。孵育18小时后,通过酶联免疫吸附测定(ELISA)检测单核细胞上清液中TNF的存在情况。与仅用培养基(无抗生素)、万古霉素或克林霉素孵育的细菌相比,与β-内酰胺类抗生素孵育的细菌的上清液诱导出更高水平的TNF。人血清增强了上清液诱导的TNF释放,尤其是在β-内酰胺类上清液中。通过抑制ELISA估算的上清液中可溶性肽聚糖和磷壁酸含量,以及对于肽聚糖而言通过用万古霉素-琼脂糖凝胶进行亲和去除估算的含量,均与TNF释放成正比。观察到不同抗生素从表皮葡萄球菌产生TNF释放产物的能力存在差异,其中最有效的抗生素是青霉素和苯唑西林。

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Supernatants from Staphylococcus epidermidis grown in the presence of different antibiotics induce differential release of tumor necrosis factor alpha from human monocytes.在不同抗生素存在下培养的表皮葡萄球菌的上清液可诱导人单核细胞中肿瘤坏死因子α的不同释放。
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2
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本文引用的文献

1
Intracellular pathways involved in tumor necrosis factor-alpha release by human monocytes on stimulation with lipopolysaccharide or staphylococcal peptidoglycan are partly similar.人类单核细胞在脂多糖或葡萄球菌肽聚糖刺激下释放肿瘤坏死因子-α 所涉及的细胞内途径部分相似。
J Infect Dis. 1996 Jan;173(1):212-8. doi: 10.1093/infdis/173.1.212.
2
Lipopolysaccharide and peptidoglycan share binding sites on human peripheral blood monocytes.脂多糖和肽聚糖在人外周血单核细胞上共享结合位点。
J Infect Dis. 1993 Jul;168(1):135-42. doi: 10.1093/infdis/168.1.135.
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Methods for measurement of antibody/antigen affinity based on ELISA and RIA.基于酶联免疫吸附测定法(ELISA)和放射免疫测定法(RIA)的抗体/抗原亲和力测量方法。
Curr Opin Immunol. 1993 Apr;5(2):278-81. doi: 10.1016/0952-7915(93)90018-n.
4
Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection.缺乏55kd肿瘤坏死因子受体的小鼠对内毒素休克具有抗性,但会死于单核细胞增生李斯特菌感染。
Cell. 1993 May 7;73(3):457-67. doi: 10.1016/0092-8674(93)90134-c.
5
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FEMS Immunol Med Microbiol. 1993 Oct;7(3):281-7. doi: 10.1111/j.1574-695X.1993.tb00409.x.
6
Serum-induced potentiation of tumor necrosis factor alpha production by human monocytes in response to staphylococcal peptidoglycan: involvement of different serum factors.血清诱导人单核细胞对葡萄球菌肽聚糖产生肿瘤坏死因子α的增强作用:不同血清因子的参与
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7
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Infect Immun. 1994 Nov;62(11):4975-80. doi: 10.1128/iai.62.11.4975-4980.1994.
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Infect Immun. 1994 Nov;62(11):4709-15. doi: 10.1128/iai.62.11.4709-4715.1994.