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Inflammatory Response01:28

Inflammatory Response

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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.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
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Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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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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Inflammation01:38

Inflammation

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Overview
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Inflammatory Response II: Inflammatory Exudate and Tissue Repair01:24

Inflammatory Response II: Inflammatory Exudate and Tissue Repair

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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.
The typical wound exudate is odorless, transparent, straw-colored, thin, and watery. Exudate, however, can differ depending on the state of wound healing. Likewise, the...
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Phases of Wound Repair01:28

Phases of Wound Repair

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Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...
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Tissue Injury: Inflammation and Repair01:28

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Related Experiment Video

Updated: Apr 5, 2026

Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses
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Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses

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Sweet NETs, Bitter Wounds.

Venizelos Papayannopoulos1

  • 1Mill Hill laboratories, The Francis Crick Institute, London NW7 1AA, UK.

Immunity
|August 20, 2015
PubMed
Summary
This summary is machine-generated.

Hyperglycemia in diabetes increases neutrophil extracellular traps, which are shown to slow wound healing. This finding helps understand why diabetic wounds heal poorly.

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Area of Science:

  • Biomedical Science
  • Wound Healing Research
  • Diabetes Complications

Background:

  • Diabetic wound healing is a significant clinical challenge.
  • The underlying mechanisms contributing to delayed healing in diabetes remain incompletely understood.
  • Neutrophil extracellular traps (NETs) are implicated in inflammatory processes.

Purpose of the Study:

  • To investigate the role of neutrophil extracellular traps (NETs) in the impaired wound healing observed in diabetes.
  • To elucidate the association between hyperglycemia and NETs deployment in the context of wound repair.

Main Methods:

  • The study by Wong et al. (2015) examined the deployment of neutrophil extracellular traps in diabetic wound models.
  • Analysis focused on the correlation between hyperglycemia levels and NETs formation.

Main Results:

  • An increased deployment of neutrophil extracellular traps was observed in the context of hyperglycemia.
  • This heightened NETs activity was directly linked to a reduction in wound healing rates.

Conclusions:

  • Increased neutrophil extracellular trap deployment, driven by hyperglycemia, is a key factor contributing to slow wound healing in diabetes.
  • Targeting NETs formation may offer a therapeutic strategy for improving diabetic wound repair.