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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...
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T Cell Types and Functions

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Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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...
Encephalitis ll: Pathophysiology01:26

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Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

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Acute Inflammation II: Cellular Phase

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Related Experiment Video

Updated: Jun 5, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:22

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Post-stroke infection: a role for IL-1ra?

Pat Tanzi1, Kevin Cain, Angela Kalil

  • 1Department of Neurology, University of Washington, School of Medicine, Harborview Medical Center, Box 359775, 325 9th Ave, Seattle, WA 98104-2499, USA.

Neurocritical Care
|December 22, 2010
PubMed
Summary

Post-stroke infections are common and linked to poor outcomes. This study found Interleukin-1 receptor antagonist (IL-1ra) is independently associated with increased infection risk after stroke.

Related Experiment Videos

Last Updated: Jun 5, 2026

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
08:22

Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model

Published on: June 20, 2025

Area of Science:

  • Neuroscience
  • Immunology
  • Clinical Medicine

Background:

  • Infection post-stroke is a significant complication, worsening patient outcomes.
  • Stroke-induced immunologic dysfunction may increase infection susceptibility.
  • The role of cytokines and hormones in post-stroke infection risk requires further investigation.

Purpose of the Study:

  • To investigate the association between immunomodulatory cytokines, hormones, lymphocyte function, and infection risk in stroke patients.
  • To explore the independent contribution of these factors to post-stroke infections.

Main Methods:

  • 112 ischemic stroke patients were enrolled shortly after stroke onset.
  • Blood samples were analyzed for cortisol, IL-10, IL-1ra, and lymphocyte counts/function at 72 hours post-stroke.
  • Infections were monitored up to 21 days post-stroke.

Main Results:

  • Infection occurred in 25% of patients, with stroke severity being the primary predictor.
  • Elevated plasma cortisol, IL-10, IL-1ra, and reduced lymphocyte numbers correlated with infection risk.
  • After adjusting for stroke severity, only IL-1ra remained independently associated with infection risk.

Conclusions:

  • Increased plasma IL-1ra levels are independently linked to a higher risk of infection following stroke.
  • This finding suggests IL-1ra may serve as a potential biomarker for post-stroke infection.
  • Further research is warranted to confirm these implications for future stroke therapies.