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The hosts' susceptibility to infection depends on several factors. The integrity of the skin and mucous membranes helps protect the body against microbial attacks. When the skin is altered, the chance of infection, limb loss, and even death increases.
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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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Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
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Sepsis and immune response.

Xing-Hai Chen1, Yong-Jie Yin1, Jing-Xiao Zhang1

  • 1Department of Emergency Medicine, Second Hospital of Jilin University, Changchun 130041, China.

World Journal of Emergency Medicine
|September 13, 2014
PubMed
Summary
This summary is machine-generated.

Sepsis pathogenesis remains unclear, particularly immune system dysfunction. This review examines immune responses, regulation, and inflammatory mediators in sepsis, highlighting the need for individualized treatment approaches.

Keywords:
Immune responseInflammatory mediatorSepsis

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Area of Science:

  • Critical Care Medicine
  • Immunology
  • Pathophysiology

Background:

  • Sepsis and multiple organ failure are leading causes of death in critically ill patients.
  • The precise pathogenesis of sepsis, especially immune system dysfunction, requires further elucidation.
  • Understanding immune responses and inflammatory mediators is crucial for sepsis management.

Purpose of the Study:

  • To review the immune response and regulation in sepsis.
  • To examine the functions of various inflammatory mediators in sepsis.
  • To synthesize current knowledge on sepsis pathogenesis and immune involvement.

Main Methods:

  • Systematic review of studies identified through MEDLINE and PubMed searches.
  • Keywords used: "sepsis", "immune response", "inflammatory mediator".
  • Manual search of references from key articles to ensure comprehensive data collection.

Main Results:

  • The review covered immune response, immune regulation, inflammatory mediators, high-mobility group box 1 protein, complement system, and autonomic nervous system.
  • No current therapeutic strategies effectively target the inflammatory response in sepsis.
  • Mortality rates for sepsis have not shown significant reduction.

Conclusions:

  • Sepsis is a complex, dynamic condition encompassing heterogeneous syndromes.
  • Individualized treatment is essential due to variations in etiology, susceptibility, and patient responses.
  • Further research into sepsis pathogenesis and targeted therapies is warranted.