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Related Concept Videos

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect...
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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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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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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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Related Experiment Video

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Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury
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Complement mediates a primed inflammatory response after traumatic lung injury.

J Jason Hoth1, Jonathan D Wells, Sarah E Jones

  • 1From the Department of General Surgery (J.J.H., J.D.W., B.K.Y.), and Section on Molecular Medicine (C.E.M.), Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, North Carolina.

The Journal of Trauma and Acute Care Surgery
|February 21, 2014
PubMed
Summary
This summary is machine-generated.

Pulmonary contusion (PC) primes the immune system for infection. Thrombin activates complement C5a after PC, increasing inflammation. Inhibiting thrombin or C5a reduces this immune priming effect.

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Area of Science:

  • Immunology
  • Trauma Research
  • Complement System Biology

Background:

  • Pulmonary contusion (PC) is a severe injury that can prime the immune system for exaggerated responses to subsequent infections.
  • The role of complement (C) activation in PC-induced immune priming is not fully understood.

Purpose of the Study:

  • To investigate the hypothesis that PC-induced complement activation contributes to immune priming for a secondary insult.
  • To explore the role of thrombin in complement activation following PC.

Main Methods:

  • Male C57BL/6 mice underwent blunt chest trauma to induce PC.
  • Inflammatory markers, including complement C5a, were measured in tissue, serum, and bronchoalveolar lavage (BAL) at various time points post-injury.
  • Thrombin activity was inhibited using hirudin to assess its role in C activation.
  • Primed responses were evaluated by challenging injured mice with lipopolysaccharide (LPS) as a second hit.

Main Results:

  • Elevated C5a levels were observed in the BAL of PC mice, persisting for up to 72 hours post-injury.
  • Inhibition of thrombin significantly reduced C5a levels in injured mice.
  • PC mice challenged with LPS exhibited heightened inflammatory responses and increased C5a.
  • Inhibition of C5a or its receptor, or C5a deficiency, attenuated the primed inflammatory response to LPS.

Conclusions:

  • Complement C5a is elevated for several days after PC, indicating sustained activation.
  • Thrombin-induced complement activation appears to be a major pathway following PC.
  • Inhibiting C5a effectively reduces the injury-primed inflammatory response to secondary challenges like LPS.
  • These findings highlight a significant cross-talk between coagulation and complement systems in mediating immune priming after PC.