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Inflammatory Response01:28

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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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Inflammatory Response I: Vascular and Cellular01:30

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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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The immune system's inflammatory response destroys the invading pathogen, permitting the tissue to heal. The changes during the cellular and vascular stages allow exudate formation at the site of inflammation. The inflammatory exudate released from the wound has high protein content and a specific gravity above 1.020.
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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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A Feedback Loop between Inflammation and Zn Uptake.

Paola Bonaventura1, Aline Lamboux2, Francis Albarède2

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Inflammation from cytokines like IL-17 and TNF-α increases zinc uptake in cells, which can worsen inflammation. This creates a feedback loop between zinc levels and immune responses.

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Area of Science:

  • Immunology
  • Cell Biology
  • Nutritional Biochemistry

Background:

  • Zinc (Zn) plays a critical role in immune function.
  • Systemic zinc deficiency is linked to inflammation.
  • Chronic inflammatory conditions like rheumatoid arthritis (RA) may involve altered cellular zinc metabolism.

Purpose of the Study:

  • To investigate how inflammation affects cellular zinc metabolism.
  • To model chronic inflammation using rheumatoid arthritis (RA) synoviocytes exposed to cytokines.
  • To compare inflammatory synoviocytes with osteoarthritis (OA) synoviocytes as controls.

Main Methods:

  • Measured intracellular and extracellular zinc levels using ICP-MS with a stable zinc isotope.
  • Assessed gene expression of zinc transporter ZIP-8, exporter ZnT1, and metallothioneins (MTs).
  • Quantified IL-6 production as an inflammation marker via ELISA.

Main Results:

  • Pro-inflammatory cytokines (IL-17 and TNF-α) upregulated the zinc importer ZIP-8.
  • Zinc exporter ZnT1 and MT expression were dependent on extracellular zinc concentrations.
  • Exogenous zinc addition amplified IL-6 production, indicating a positive feedback loop.

Conclusions:

  • Cytokine-mediated inflammation enhances zinc uptake in synoviocytes.
  • A feedback loop exists where inflammation increases zinc uptake, further promoting inflammation.
  • Developed a mathematical model for cytokine-mediated alterations in zinc homeostasis.