Classically Activated M1 Macrophage Identification Service

Macrophages commonly exist in two distinct subsets: classically activated macrophages (M1) and alternatively activated macrophages (M2). M1 macrophages can facilitate immunity to remove foreign pathogens and tumor cells, mediate tissue damage, impair wound healing and tissue regeneration. A better understanding of the molecular pathways and transcriptional programs associated with M1 macrophage subtypes, as well as reliable markers, is necessary for further progress in the M1 macrophage field. Creative Biolabs is well-equipped and versed in the identification of M1 macrophages based on our clients' requirements. We are glad to serve our global clients with professionalism and expertise in M1 macrophage identification.

Introduction of M1 Macrophages

Macrophages play an important role in a wide variety of physiologic and pathologic processes. Plasticity and functional polarization are hallmarks of macrophages. As one of the two important subsets, M1 macrophages are typically induced by bacterial LPS or by some cytokines, such as Interferon-gamma (IFN-γ), tumor necrosis factor-alpha (TNF-α), and granulocyte-macrophage colony-stimulating factor (GM-CSF). M1 macrophages are characterized by high proinflammatory cytokine production, high chemokine (C-X-C motif) ligand 9 (CXCL9) production, and low levels of interleukin (IL)-10. Efficient M1 macrophage responses are important for ensuring resistance to bacterial infection. Many pathogens such as Brucella, Salmonella, and Mycobacterium have evolved mechanisms that interfere with M1 polarization. Conversely, excessive or unresolved M1 macrophage activation can cause chronic inflammation and tissue damage. Studies have shown that M1 macrophages are related to the pathogenesis of atherosclerosis, diabetes, and glomerulonephritis. In the nervous system, M1 macrophages have been associated with multiple sclerosis, amyotrophic lateral sclerosis, stroke, spinal cord injury, and traumatic brain injury.

M1 Macrophage Identification Service at Creative Biolabs

Identification of M1subsets at Creative Biolabs is usually carried out by quantification of M1 macrophage markers, including multiple cell surface markers, transcription factors, and cytokine profiles. IFN-γ, IL-1, IL-6, IL-10, IL-12, IL-23, TNF-α, CD16, CD32, CD64, CD68, CD80, CD86, CD369, inducible nitric oxide synthase (iNOS), signal transducer and activator of transcription 1 (STAT1), interferon regulatory factor 5 (IRF5), Mer tyrosine kinase (MerTK), class II major histocompatibility complex molecules (MHC class II), and CXCL9 are reliable markers for human M1 macrophages, while IFN-γ, IL-1, IL-6  IL-10,IL-12, IL-23, TNF-α, CD14, CD16, CD32, CD64, CD68, CD80, CD86, CD204, CD369, IRF5, MerTK, MHC II, and Ly-6C are often used for the identification of mouse M1 macrophages. Based on our powerful Macrophage Therapeutics Development Platform, our scientists are proficient at applying real-time PCR for transcriptional signature analysis, liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteome analysis, western blot (WB), immunohistochemistry (IHC), and flow cytometry (FC) for a comprehensive analysis of M1 macrophages.

Classically Activated M1 Macrophage Identification Service

Moreover, our R&D scientific team has developed machine learning algorithms to automatedly identify M1 macrophage functional phenotypes using their cell size and morphology. Then, fluorescent microscopy will be performed to assess the cell morphology of M1 macrophages.

Equipped with a team of seasoned scientists and advanced facilities, Creative Biolabs offers fast, reliable support for M1 macrophage identification to facilitate our clients' macrophage development projects. For more detailed information on M1 macrophage identification, please contact us for more information and a detailed quote.

Reference

  1. Zhu, Y.; et al. Identification of different macrophage subpopulations with distinct activities in a mouse model of oxygen-induced retinopathy. International journal of molecular medicine. 2017, 40(2):281-92.
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