NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.

NO is a macrophage autonomous modifier of the cytokine response to streptococcal single-stranded RNA.
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DOI:
10.4049/jimmunol.1101383
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发表时间:
2012-01-15
期刊:
Journal of immunology (Baltimore, Md. : 1950)
影响因子:
--
通讯作者:
Henneke P
Henneke P
中科院分区:
其他
文献类型:
--
作者:
Deshmukh SD;Müller S;Hese K;Rauch KS;Wennekamp J;Takeuchi O;Akira S;Golenbock DT;Henneke P

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B组链球菌(GBS)是脓毒症的主要原因,其诱导的炎性细胞因子严格依赖于细菌ssRNA和宿主分子MyD 88和MyD-93 B。在这里,我们表明,一氧化氮在GBS诱导的细胞因子基因的转录激活中起着重要作用。吞噬作用以MyD 88依赖的方式诱导NO。反过来,NO传播吞噬体的酸化和吞噬体细菌核酸的加工,并且是链球菌对细胞因子基因的有效转录激活所需的。这种NO依赖性放大环对抗链球菌巨噬细胞反应和脓毒症发病机制具有重要的机制意义。
Group B streptococcus (GBS), a major cause of sepsis, induces inflammatory cytokines in strict dependence of bacterial ssRNA and the host molecules MyD88 und UNC-93B. Here, we show that nitric oxide plays an important role in GBS-induced transcriptional activation of cytokine genes. Phagocytosis induced NO in a MyD88-dependent fashion. In turn, NO propagated the acidification of phagosomes and the processing of phagosomal bacterial nucleic acids and was required for potent transcriptional activation of cytokine genes by streptococci. This NO-dependent amplification loop has important mechanistic implications for the anti-streptococcal macrophage response and sepsis pathogenesis.
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