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与自体血小板相互作用会使单核细胞中白细胞介素 -1 和肿瘤坏死因子的产生增加。

Interaction with autologous platelets multiplies interleukin-1 and tumor necrosis factor production in mononuclear cells.

作者信息

Aiura K, Clark B D, Dinarello C A, Margolis N H, Kaplanski G, Burke J F, Tompkins R G, Gelfand J A

机构信息

Department of Medicine, Tufts University School of Medicine and New England Medical Center, Boston, MA 02111, USA.

出版信息

J Infect Dis. 1997 Jan;175(1):123-9. doi: 10.1093/infdis/175.1.123.

Abstract

The effect of activated platelets on cytokine production by human peripheral blood mononuclear cells (PBMC) was investigated. When PBMC were coincubated with activated autologous platelets amid lipopolysaccharide (LPS, 50-100 pg/mL) for 8 h, the production of interleukin (IL)-1alpha increased 11- to 18-fold and tumor necrosis factor (TNF)-alpha 3- to 5-fold compared with PBMC without platelets. Activated platelets in a dual-chamber well that prevented platelet-PBMC contact but permitted passage of soluble factors enhanced IL-1alpha production (P < .01). Platelet-PBMC contact in the chamber resulted in a further enhancement of IL-1alpha production. These data suggest that platelet-PBMC interaction, both directly and with platelet-derived factors, enhances production of shock-producing IL-1alpha and TNF-alpha, albeit differently. The interaction of platelets with monocytes may play an important role in the pathophysiology of sepsis and disseminated intravascular coagulation.

摘要

研究了活化血小板对人外周血单个核细胞(PBMC)细胞因子产生的影响。当PBMC与脂多糖(LPS,50 - 100 pg/mL)存在下的活化自体血小板共孵育8小时时,与无血小板的PBMC相比,白细胞介素(IL)-1α的产生增加了11至18倍,肿瘤坏死因子(TNF)-α增加了3至5倍。在双腔孔中活化的血小板可防止血小板与PBMC接触,但允许可溶性因子通过,从而增强了IL-1α的产生(P < 0.01)。腔室内血小板与PBMC的接触导致IL-1α产生进一步增强。这些数据表明,血小板与PBMC的相互作用,无论是直接的还是与血小板衍生因子的相互作用,都会增强产生休克的IL-1α和TNF-α的产生,尽管方式不同。血小板与单核细胞的相互作用可能在脓毒症和弥散性血管内凝血的病理生理学中起重要作用。

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