Related Experiment Video

Updated: Jun 6, 2026

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
07:30

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Sepsis induces early alterations in innate immunity that impact mortality to secondary infection

Matthew J Delano1, Terri Thayer, Sonia Gabrilovich

  • 1Department of Surgery, College of Medicine, University of Florida Health Science Center, Gainesville, FL 32610, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|November 26, 2010
PubMed

Insights

Sepsis impairs neutrophil function, increasing susceptibility to secondary bacterial pneumonia. However, it enhances monocyte responses, reducing susceptibility to Listeria infections.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Microbiology

Background:

  • Sepsis, a life-threatening systemic inflammatory response to infection, alters immune function.
  • This immune dysregulation is thought to increase susceptibility to subsequent infections and organ failure.

Purpose of the Study:

  • To investigate how sepsis affects susceptibility to distinct secondary infections.
  • To define the immune mechanisms underlying these altered susceptibilities.

Main Methods:

  • A murine model of polymicrobial sepsis was used.
  • Mice were subsequently infected with Pseudomonas aeruginosa (pneumonia) or Listeria monocytogenes (disseminated).
  • Immune cell populations (neutrophils, monocytes) and survival rates were assessed.

Main Results:

  • Early after sepsis, neutrophil numbers and function were reduced, increasing mortality from P. aeruginosa pneumonia.
  • Monocyte recruitment and function were enhanced via the CCR2/MCP-1 pathway.
  • Mortality from L. monocytogenes infection, dependent on monocytes/macrophages, was decreased post-sepsis.

Conclusions:

  • Sepsis causes pathogen-specific alterations in innate immunity.
  • Early neutrophil impairment drives increased susceptibility to certain secondary bacterial infections.
  • Enhanced monocyte function may offer protection against other infections like listeriosis.

More Related Videos

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis14:54

A Controlled Mouse Model for Neonatal Polymicrobial Sepsis

Published on: January 27, 2019

A Data-Driven Approach to Quantifying Immune States in Sepsis07:42

A Data-Driven Approach to Quantifying Immune States in Sepsis

Published on: February 7, 2025

Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

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...
Factors Affecting the Risk of Infection01:26

Factors Affecting the Risk of Infection

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.
The integrity and count of the white blood cells help the body resist pathogens and fight infection. When impaired, it reduces the body's resistance to pathogens. The acidic pH levels of the gastrointestinal, genitourinary tracts, and skin create...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Determinants of Bacterial Pathogenicity and Virulence01:20

Determinants of Bacterial Pathogenicity and Virulence

Pathogenic bacteria employ a variety of strategies to establish infections, including the secretion of extracellular enzymes that act as potent virulence factors. These enzymes facilitate bacterial colonization of host tissues and help evade immune surveillance. By targeting structural components of host tissues and interfering with immune mechanisms, these enzymes play a pivotal role in disease progression.Extracellular Enzymes Facilitating Tissue Invasion: Several bacterial pathogens secrete...
Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
Stages of Infection01:26

Stages of Infection

Stages of infection describe what happens to a susceptible host once a pathogen invades the human body. The stages of infection are incubation, prodromal, illness, stage of decline, and convalescence. The incubation stage is the period from exposure to a pathogen until symptoms start. The infected person is unaware of impending illness as the pathogens grow and multiply within the body. The duration may vary depending on the type of infection. The incubation period of measles averages ten to...