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Related Concept Videos

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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Inflammation01:38

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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.
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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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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
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Vascular Spasm01:16

Vascular Spasm

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The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last...
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Related Experiment Video

Updated: Oct 15, 2025

Bronchoalveolar Lavage Exosomes in Lipopolysaccharide-induced Septic Lung Injury
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Small Extracellular Vesicles Propagate the Inflammatory Response After Trauma.

Tanja Seibold1, Jonathan Schönfelder1, Florian Weeber1

  • 1Department of Internal Medicine I, University Hospital Ulm, Albert-Einstein-Allee 23, Ulm, 89081, Germany.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|October 29, 2021
PubMed
Summary

Trauma-related deaths, especially from thorax trauma, are linked to inflammation driven by small extracellular vesicles (sEVs). Inhibiting sEVs reduces inflammation and organ damage, highlighting their role in polytrauma.

Keywords:
endotheliuminflammationneutrophilssmall extracellular vesiclestrauma

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Area of Science:

  • Traumatology
  • Immunology
  • Cell Biology

Background:

  • Trauma, particularly thorax trauma (TxT), is a leading cause of death in young adults.
  • TxT is associated with severe outcomes like sepsis, ARDS, and multiple organ dysfunction.
  • Uncontrolled inflammation and endothelial activation are key features of severe trauma.

Purpose of the Study:

  • To investigate the role of small extracellular nanovesicles (sEVs) in mediating inflammation and organ damage following trauma.
  • To explore sEVs as potential therapeutic targets for mitigating trauma-induced complications.

Main Methods:

  • Induction of in vivo trauma (TxT) and in vitro polytrauma cytokine cocktails.
  • Analysis of sEV release from endothelial cells and their cargo.
  • Inhibition of sEV release in a mouse model of TxT.
  • Administration of TxT-plasma-sEVs to healthy animals.
  • Assessment of inflammatory markers, neutrophil infiltration, and organ damage (AKI).

Main Results:

  • Trauma triggers the release of pro-inflammatory sEVs from endothelial cells.
  • These sEVs carry transcripts (ICAM-1, VCAM-1, E-selectin, cytokines) that activate endothelium and promote inflammation.
  • Inhibiting sEV release in mice reduced local and systemic inflammation and kidney injury.
  • Transfer of TxT-plasma-sEVs induced inflammation and AKI in healthy animals.
  • Elevated sEV levels and similar cargo were found in polytrauma patients.

Conclusions:

  • sEVs play a critical role in mediating systemic inflammation and organ damage after trauma.
  • sEV-mediated transfer of inflammatory cargo is a fundamental mechanism in polytrauma pathophysiology.
  • Targeting sEV release or function presents a promising therapeutic strategy for trauma patients.