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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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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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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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
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Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1&beta; using a Whole Blood Stimulation Assay
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Accurate and Simple Measurement of the Pro-inflammatory Cytokine IL-1β using a Whole Blood Stimulation Assay

Published on: March 1, 2011

Pathogen-induced interleukin-1beta processing and secretion is regulated by a biphasic redox response.

Sara Tassi1, Sonia Carta, Roberta Vené

  • 1Cell Biology Unit, National Cancer Research Institute, Genova, Italy.

Journal of Immunology (Baltimore, Md. : 1950)
|June 30, 2009
PubMed
Summary

Pathogen-associated molecular patterns trigger a biphasic redox event in monocytes, involving reactive oxygen species (ROS) and an antioxidant response, essential for interleukin-1beta (IL-1beta) secretion.

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Area of Science:

  • Immunology
  • Cellular Biology
  • Redox Biology

Background:

  • Interleukin-1beta (IL-1beta) is a key inflammatory cytokine.
  • Its processing and secretion are crucial for immune responses.
  • Pathogen-associated molecular patterns (PAMPs) are known to induce IL-1beta secretion.

Purpose of the Study:

  • To elucidate the redox mechanisms regulating PAMP-induced IL-1beta secretion in human monocytes.
  • To investigate the role of reactive oxygen species (ROS) and antioxidant responses in this process.

Main Methods:

  • Utilized human monocytes stimulated with PAMP molecules.
  • Assessed reactive oxygen species (ROS) generation using specific inhibitors (NADPH oxidase inhibitors).
  • Evaluated antioxidant responses, including thioredoxin, thioredoxin reductase, and cysteine release.
  • Investigated the impact of genetic silencing (siRNA) of key redox enzymes (thioredoxin, superoxide dismutase 1).

Main Results:

  • PAMP stimulation induced a biphasic redox event: early ROS generation followed by a delayed antioxidant response.
  • The antioxidant phase involved increased intracellular thioredoxin and released reduced cysteine.
  • Inhibition of ROS production or antioxidant pathways (thioredoxin reductase) impaired IL-1beta secretion.
  • Exogenous reducing agents restored IL-1beta secretion, indicating the importance of extracellular reduction.
  • Silencing of thioredoxin or superoxide dismutase 1 also inhibited IL-1beta secretion.

Conclusions:

  • PAMP-induced IL-1beta secretion is tightly regulated by a biphasic redox mechanism in monocytes.
  • Early ROS production acts as a trigger for a subsequent antioxidant response.
  • This antioxidant response, involving redox enzymes and cysteine release, is critical for IL-1beta processing and secretion.