EasySep™ Direct人嗜酸性粒细胞分选试剂盒

全血免疫磁珠负选试剂盒

产品号 #19656

直接从全血中通过免疫磁珠分选嗜酸性粒细胞

产品优势

  • 高效去除红细胞,无需密度梯度离心、沉降或裂解
  • 分选获得的细胞纯度高达98%
  • 易于操作、快速,且无需分离柱
  • 分选得到的细胞未被标记

产品组分包括

  • EasySep™ Direct人嗜酸性粒细胞分选试剂盒(产品号 #19656)
    • EasySep™ Direct人嗜酸性粒细胞分选抗体混合物,2 x 2.5 mL
    • EasySep™ Direct RapidSpheres™ 磁珠,4 x 2.5 mL

概述
EasySep™ Direct人嗜酸性粒细胞分选试剂盒,通过免疫磁性负选,直接从人全血中分选出具有功能的、高纯度的嗜酸性粒细胞。无需裂解、密度梯度离心或其他处理步骤,分选得到的细胞可立即用于流式细胞术、功能分析、细胞培养及其他后续应用。

MAGNET COMPATIBILITY
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
• Easy 50 EasySep™ Magnet (Catalog #18002)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
 
SUBTYPE
Cell Isolation Kits
 
CELL TYPE
Granulocytes and Subsets
 
SPECIES
Human
 
SAMPLE SOURCE
Whole Blood
 
SELECTION METHOD
Negative
 
APPLICATION
Cell Isolation
 
BRAND
EasySep
 
AREA OF INTEREST
Immunology

实验数据

Figure 1. Typical EasySep™ Direct Human Eosinophil Isolation Profile

Starting with human whole blood from normal healthy donors, the typical eosinophil (CD16-CD66b+) content of the non-lysed final isolated fraction is 95.8 ± 2.7% (gated on CD45). In the above example, the eosinophil content of the lysed whole blood start sample and the non-lysed final isolated fraction is 2.3% and 97.6% (gated on CD45), respectively, or 2.2% and 90.8% (not gated on CD45), respectively.

产品说明书及文档

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
19656
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
19656
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
19656
Lot #
All
Language
English

应用领域

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

相关材料与文献

Educational Materials (11)

Publications (1)

Neutrophils from severe asthmatic patients induce epithelial to mesenchymal transition in healthy bronchial epithelial cells. A. Haddad et al. Respiratory research 2019 oct

Abstract

BACKGROUND Asthma is a heterogenous disease characterized by chronic inflammation and airway remodeling. An increase in the severity of airway remodeling is associated with a more severe form of asthma. There is increasing interest in the epithelial to mesenchymal transition process and mechanisms involved in the differentiation and repair of the airway epithelium, especially as they apply to severe asthma. Growing evidence suggests that Epithelial-Mesenchymal transition (EMT) could contribute to airway remodeling and fibrosis in asthma. Severe asthmatic patients with remodeled airways have a neutrophil driven inflammation. Neutrophils are an important source of TGF-$\beta$1, which plays a role in recruitment and activation of inflammatory cells, extracellular matrix (ECM) production and fibrosis development, and is a potent inducer of EMT. OBJECTIVE As there is little data examining the contribution of neutrophils and/or their mediators to the induction of EMT in airway epithelial cells, the objective of this study was to better understand the potential role of neutrophils in severe asthma in regards to EMT. METHODS We used an in vitro system to investigate the neutrophil-epithelial cell interaction. We obtained peripheral blood neutrophils from severe asthmatic patients and control subjects and examined for their ability to induce EMT in primary airway epithelial cells. RESULTS Our data indicate that neutrophils from severe asthmatic patients induce changes in morphology and EMT marker expression in bronchial epithelial cells consistent with the EMT process when co-cultured. TGF-$\beta$1 levels in the culture medium of severe asthmatic patients were increased compared to that from co-cultures of non-asthmatic neutrophils and epithelial cells. CONCLUSIONS AND CLINICAL RELEVANCE As an inducer of EMT and an important source of TGF-$\beta$1, neutrophils may play a significant role in the development of airway remodeling and fibrosis in severe asthmatic airways.
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