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Introduction

Redness, hot pain as well as sepsis, are symptoms of the pathological process of infectious inflammation, a phenomenon that occurs with the participation of mediators produced by a large number of inflammatory cells, where cytokines are also involved. Cytokines are biologically active low molecular weight proteins or peptides secreted by various cells that regulate cell growth and differentiation, immune function, inflammation and wound healing. When pathogens invade or the body ages, inflammatory cytokines activate the body's immune system to defend against invaders. And when invaders are eliminated and the body needs to regain stability, anti-inflammatory cytokines are secreted. The constant interaction and balance between inflammatory and anti-inflammatory cytokines is an important part of the human immune system.

Mechanism and Function

Pro-inflammatory cytokines are endogenous peptides with powerful biological effects produced mainly by cells of the immune system, including interleukin-1β, tumor necrosis factor (TNF-α), IL-6, IL-18, IL-17 and IL-15, etc. Among them, IL-1 is capable of activating a variety of pro-inflammatory cytokines of immune and inflammatory cells, and it includes IL-1α and IL-1β. IL-1β promotes the proliferation and differentiation of B cells, mediates the secretion of immunoglobulins, and enhances the process of cellular and humoral immune-mediated tissue injury. Another typical pro-inflammatory cytokine TNF-α can stimulate macrophages, fibroblasts, smooth muscle cells, epithelial cells and endothelial cells to cause arachidonic acid metabolites and proteases, etc. It can also phagocytose cell products and complement fragments to cause cell necrosis and edema, leading to tissue damage of untouched cells. Besides, it can promote the secretion of intestinal epithelial cells and the expression of IL-8 gene, upregulate T Number of cells, eosinophils and basophils.

Inflammatory cytokines can regulate the response of pro-inflammatory cytokine production, mainly including IL-4, IL-5, IL-10, IL-13, transforming growth factor (TGF), epiodermal growth factor and so on. Among them, IL-4 can inhibit the production of other pro-inflammatory cytokines such as IL-1 and IL-6, as well as the production of lymphocytes and macrophages. IL-10 can inhibit the production of activated monocytes, macrophages, granulocytes and T cells. And IL-13 can inhibit the production of pro-inflammatory transmitters and down-regulate the function of monocytes with cytotoxicity. TGF-β can inhibit the inflammatory response of intestine. And EGF can stimulate tissue repair and protect the mucosa of gastrointestinal tract.

Creative Proteomics can provide cytokine detection platform for scientific research. According to different purposes, our dedicated analysts will customize exclusive solutions for you. We aim to provide customers with high-quality and convenient services to help you accelerate the progress of your project.

Our cytokine detection service includes but is not limited to:

Sample requirements

Our advantages:

Technology platform:

We mainly provide the Luminex cytokine detection platform. Luminex uses fluorescently encoded microspheres with specific antibodies to different target molecules. The different microspheres can be combined freely to a certain extent so that up to 100 analytes can be tested multiple times simultaneously in a single experiment.

The Luminex cytokine assay platform has the following advantages:

For your different needs, we can also provide the following detection methods:

For more information about cytokines in inflammation arthritis detection service or need other detection requirements, please contact us.

References:

  1. Zheng K Y . The Biological Functions of T Helper 17 Cell Effector Cytokines in Inflammation. Immunity, 2008.
  2. Ouyang W, Rutz S, Crellin N K, et al. Regulation and Functions of IL-10 Family Cytokines in Inflammation and Diseases. Annual Review of Immunology, 2010, 29(1):71-109.
* For Research Use Only. Do Not use in diagnostic or therapeutic procedures.

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