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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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,...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammatory Response I: Vascular and Cellular01:30

Inflammatory Response I: Vascular and Cellular

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,...
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

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 damage-associated...
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...
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...

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Related Experiment Video

Updated: Jun 18, 2026

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side
09:58

A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side

Published on: May 6, 2016

The choroid plexus response to a repeated peripheral inflammatory stimulus.

Fernanda Marques1, João C Sousa, Giovanni Coppola

  • 1Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus Gualtar, 4710-057 Braga, Portugal. fmarques@ecsaude.uminho.pt

BMC Neuroscience
|November 20, 2009
PubMed
Summary

Peripheral inflammation impacts the brain by altering choroid plexus gene expression, potentially influencing neurodegenerative diseases. This study reveals sustained changes in immune response pathways following inflammatory stimuli.

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A Choroid Plexus Epithelial Cell-based Model of the Human Blood-Cerebrospinal Fluid Barrier to Study Bacterial Infection from the Basolateral Side
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Area of Science:

  • Neuroscience
  • Immunology
  • Molecular Biology

Background:

  • Chronic systemic inflammation is linked to neurodegenerative disorders like Alzheimer's disease and multiple sclerosis.
  • The choroid plexus acts as a barrier and pathway for inflammatory signals entering the brain via cerebrospinal fluid.
  • Mechanisms by which peripheral inflammation induces central nervous system inflammation are not fully understood.

Purpose of the Study:

  • To investigate the choroid plexus gene expression profile in response to repeated peripheral inflammatory stimuli.
  • To understand how the choroid plexus responds to inflammation and potentially contributes to brain inflammation.

Main Methods:

  • Mice were administered lipopolysaccharide intraperitoneally every two weeks for three months.
  • Gene expression profiling of the mouse choroid plexus was performed using microarray analysis.
  • Mice were sacrificed 3 and 15 days post-final lipopolysaccharide injection to assess gene expression changes.

Main Results:

  • The choroid plexus demonstrated a sustained gene expression response to repeated inflammatory stimuli.
  • Significant numbers of genes were up-regulated and down-regulated at 3 and 15 days after the last injection.
  • Key affected pathways involved cell entry into cerebrospinal fluid and innate immune responses.

Conclusions:

  • The findings enhance understanding of the brain's response to peripheral inflammation.
  • This research provides a foundation for studying the role of these mechanisms in central nervous system disorders with inflammatory components.