• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Phagocytosis-mediated Ml activation by chitin but not by chitosan
【24h】

Phagocytosis-mediated Ml activation by chitin but not by chitosan

机译：吞噬症介导的丁蛋白的ML活化，但不是壳聚糖

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Chitin particles have been used to understand host response to chitin-containing pathogens and allergens and are known to induce a wide range of polarized macrophage activations, depending, at least in part, on particle size. Nonphagocytosable particles larger than a macrophage induce tissue repair M2 activation. In contrast, phagocytosable chitin microparticles (CMPs, 1-10 糾 diameters) induce Ml macrophages that kill intracellular microbes and damage tissues. However, chitosan (deacetylated) microparticles (de-CMPs, 1-10 糾) induce poor Ml activation. Toll-like receptor 2 (TLR2) and associated coreceptors in macrophages appear to be required for the Ml activation. To understand the exact mechanism of phagocytosis-mediated Ml activation by chitin, we isolated macrophage proteins that bind to CMPs during early phagocytosis and determined that TLR1, TLR2, CD14, late endosomal/lysosomal adaptor MAPK and mechanistic target of rapa-mycin activator 1 (LAMTOR1), Lck/Yes novel tyrosine kinase (Lyn), and P-actin formed phagosomal CMP-TLR2 clusters. These proteins were also detected in TLR2 phagosomal clusters in macrophages phagocytosing de-CMPs, but at relatively lower levels than in the CMP-TLR2 clusters. Importantly, CMP-TLR2 clusters further recruited myeloid differentiation primary response gene 88 (MyD88) and Toll-IL-1 receptor-containing adaptor protein (TIRAP) and phos-phorylated Lyn, whereas neither the adaptors nor phosphorylated Lyn was detected in the de-CMP clusters. The results indicate that the acetyl group played an obligatory, phagocytosis-dependent role in the initiation of an integrated signal for TLR2-mediated Ml activation.
机译：几丁质颗粒已被用于了解宿主反应对含丁肽的病原体和过敏原，并且已知诱导宽范围的偏振巨噬细胞活化，至少部分地对粒度。非巨噬细胞颗粒大于巨噬细胞诱导组织修复M2活化。相反，吞噬细胞蛋白微粒（CMP，1-10直径）诱导杀死细胞内微生物和损伤组织的ML巨噬细胞。然而，壳聚糖（脱乙酰化）微粒（DE-CMPS，1-10℃）诱导差的ML活化。 ML活化需要巨大的受体2（TLR2）和相关的巨噬细胞中的相关团簇。要了解龟蛋白介导的ML活化的确切机制，我们将在早期吞噬作用期间与CMP结合的巨噬细胞蛋白质分离，并确定了RLR1，TLR2，CD14，晚期内体/溶酶体衔接子MAPK和RAPA-Mycin活化剂1的机械靶标（ LAMTOR1），LCK /是新型酪氨酸激酶（LYN）和P-肌动蛋白形成噬菌体CMP-TLR2簇。这些蛋白质也被检测在TLR2噬菌体簇中的巨噬细胞吞噬细胞DE-CMPS，但在比CMP-TLR2簇中的水平相对较低。重要的是，CMP-TLR2簇进一步募集髓样分化初级反应基因88（MYD88）和含Toll-IL-1受体的适配器蛋白（TIRAP）和PHOS-Phorylated LIN，而适应剂也不在DE-中检测到磷酸化LYN。 CMP集群。结果表明，乙酰基在为TLR2介导的ML活化的集成信号引发中发挥了义务，吞噬作用依赖性作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号