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首页> 外文期刊>International journal of pediatric otorhinolaryngology >Interleukin-8 induction via NF-kappaB, p38 mitogen-activated protein kinase and extracellular signal-regulated kinase1/2 pathways in human peripheral blood mononuclear cells by Alloiococcus otitidis.
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Interleukin-8 induction via NF-kappaB, p38 mitogen-activated protein kinase and extracellular signal-regulated kinase1/2 pathways in human peripheral blood mononuclear cells by Alloiococcus otitidis.

机译:OTAllococcus otitidis通过人外周血单核细胞中的NF-κB,p38丝裂原活化蛋白激酶和细胞外信号调节激酶1/2途径诱导白介素8。

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摘要

Alloiococcus otitidis is a newly recognized species of gram-positive bacteria frequently associated with otitis media. Although immunostimulating activity of this organism has been investigated, little is known about the signaling pathways of chemokine/cytokine induction by this organism. We investigated the role of NF-kappaB and mitogen-activated protein (MAP) kinases in chemokine interleukin-8 (IL-8) production by human peripheral blood mononuclear cells (PBMCs) after stimulation with A. otitidis. The organism could induce in vitro IL-8 production in human PBMCs. IkappaBalpha, NF-kappaB, p38 MAP kinase, p44/42 MAP kinase (ERK1/2) became phosphorylated in PBMCs after stimulation with A. otitidis. And, inhibitors of NF-kappaB (caffeic acid phenylethyl ester), p38 (SB 203580), or ERK1/2 (PD 98059) significantly reduced IL-8 induction by the organism. These results were similar to findings in IL-8 induction by Streptococcus pneumoniae, another gram-positive major middle ear pathogen. Our preliminary study suggests that multiple pathways including NF-kappaB, p38, and ERK1/2 were simultaneously activated, and were associated with IL-8 induction by A. otitidis in human PBMCs.
机译:耳Alloiococcus otitidis是一种新发现的革兰氏阳性细菌,常与中耳炎有关。尽管已经研究了该生物体的免疫刺激活性,但是关于该生物体趋化因子/细胞因子诱导的信号传导途径知之甚少。我们调查了人外周血单核细胞刺激后,人外周血单核细胞(PBMC)产生的趋化因子白细胞介素8(IL-8)中的NF-κB和丝裂原激活蛋白(MAP)激酶的作用。该生物体可以诱导人PBMC体外产生IL-8。在用奥氏假单胞菌刺激后,PBMC中的IkappaBalpha,NF-kappaB,p38 MAP激酶,p44 / 42 MAP激酶(ERK1 / 2)被磷酸化。而且,NF-κB(咖啡酸苯乙基酯),p38(SB 203580)或ERK1 / 2(PD 98059)的抑制剂可显着降低生物体对IL-8的诱导作用。这些结果类似于另一种革兰氏阳性主要中耳病原体肺炎链球菌诱导IL-8的发现。我们的初步研究表明,包括NF-κB,p38和ERK1 / 2在内的多种途径均被同时激活,并与人PBMC中的A. otitidis诱导IL-8相关。

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