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首页> 外文期刊>Cytokine >Regulation of activin A release from murine bone marrow-derived neutrophil precursors by tumour necrosis factor-α and insulin
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Regulation of activin A release from murine bone marrow-derived neutrophil precursors by tumour necrosis factor-α and insulin

机译：通过肿瘤坏死因子-α和胰岛素调节来自鼠骨髓衍生的中性粒细胞前体的释放

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摘要

Activin A, a transforming growth factor-β family cytokine, plays a crucial role in regulating the onset and severity of many inflammatory conditions, such as acute lipopolysaccharide (LPS)-induced inflammation. Activin A is also implicated in type 2 diabetes (T2D), a disease characterised by insulin resistance, hyperglycaemia and chronic elevation of pro-inflammatory cytokines, including tumour necrosis factor (TNF-α). In the human, neutrophils contain activin A that can be released in response to TNF-α. Studies of inflammatory disease in vivo, however, generally use the mouse, so it is essential to know if murine neutrophils have similar properties. Regulation of activin A was investigated in bone marrow-derived neutrophil precursors (BMNPs) from 8 to 10. weeks old C57BL6/J male mice. The BMNPs contained 7-fold higher concentrations of activin A than bone marrow mononuclear cells. Release of activin A from isolated BMNPs was stimulated by TNF-α, but this was not due to increased activin A production. In contrast to TNF-α, LPS had no effect on isolated BMNPs, but stimulated activin A release and production in total bone marrow cell cultures. Moreover, activin A release in response to LPS, was not prevented in TNF-α null mice. Increased glucose and insulin had no effect on base-line activin A secretion by BMNPs in culture, but pre-treatment with insulin blocked the TNF-α induced release of activin A. These results indicate that murine neutrophils are a source of stored activin A, the release of which can be directly stimulated by TNF-α, although TNF-α is not the only stimulator of activin A release during inflammation. Furthermore, regulation of neutrophil activin A release by insulin may also play a role in the inflammation associated with T2D.
机译：Activin A，转化生长因子-β家族细胞因子在调节许多炎症病症的发作和严重程度方面起着至关重要的作用，例如急性脂多糖（LPS）诱导的炎症。 Actiacin A也涉及2型糖尿病（T2D），其疾病，其特征在于胰岛素抵抗，高血糖和促炎细胞因子的慢性升高，包括肿瘤坏死因子（TNF-α）。在人中，中性粒细胞含有可响应于TNF-α的活性素A.然而，体内炎症疾病的研究通常使用鼠标，所以必须知道小鼠中性粒细胞是否具有相似的性质。在骨髓衍生的嗜中性粒细胞前体（BMNP）中研究了激活素A的调节，从8-10岁的C57BL6 / J雄性小鼠中进行。 BMNPS含有7倍的浓度A比骨髓单核细胞。通过TNF-α刺激来自分离的BMNP的活性素A的释放，但是由于产生的激活素增加，这不是由于产生的增加。与TNF-α相反，LPS对分离的BMNP没有影响，但刺激了激活素在总骨髓细胞培养物中的释放和生产。此外，在TNF-α含氟小鼠中不能防止响应于LPS的释放。增加的葡萄糖和胰岛素对培养基的BMNP分泌没有影响碱基 - 碱基激活素，但用胰岛素预处理阻断TNF-α诱导的活性素A的释放。这些结果表明鼠中性粒细胞是储存的激活素A的来源，释放可以通过TNF-α直接刺激，尽管TNF-α不是炎症期间释放释放的唯一刺激器。此外，胰岛素释放的中性粒细胞激活素的调节也可能在与T2D相关的炎症中起作用。

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