Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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...
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...
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...
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,...
Viral Meningitis01:18

Viral Meningitis

Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Multilevel surveillance of antimicrobial resistance in Escherichia coli and Klebsiella pneumoniae from companion animals: Evidence from a Veterinary University Hospital before and after EU Regulation 2022/1255.

Veterinary microbiology·2026
Same author

Association between abdominal muscle weakness and weaning failure in mechanically ventilated critically ill patients: an ultrasound assessment.

Journal of anesthesia, analgesia and critical care·2026
Same author

High Frequency of Detection of NDM-Producing Enterobacterales Among Companion Animals Hospitalized in an Italian Veterinary Teaching Hospital.

Transboundary and emerging diseases·2025
Same author

Could honey bees signal the spread of antimicrobial resistance in the environment?

Letters in applied microbiology·2020
Same author

First description of Streptococcus lutetiensis from a diseased cat.

Letters in applied microbiology·2019
Same author

Daptomycin Plasma and CSF Levels in Patients with Healthcare-Associated Meningitis.

Neurocritical care·2019

Related Experiment Video

Updated: Jul 7, 2026

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

Central nervous system inflammation.

S G Soriano1, S Piva

  • 1Harvard Medical School, Children's Hospital Boston, Perioperative and Pain Medicine, Boston, MA, USA. sulpicio.soriano@childrens.harvard.edu

European Journal of Anaesthesiology. Supplement
|April 17, 2008
PubMed
Summary
This summary is machine-generated.

Inflammation, driven by cytokines and adhesion molecules, follows acute injury. Targeting these adhesion molecules offers potential therapeutic strategies for neurological damage.

More Related Videos

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells
09:35

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells

Published on: May 19, 2020

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Related Experiment Videos

Last Updated: Jul 7, 2026

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation
09:19

Improved 3D Hydrogel Cultures of Primary Glial Cells for In Vitro Modelling of Neuroinflammation

Published on: December 8, 2017

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells
09:35

Isolating Central Nervous System Tissues and Associated Meninges for the Downstream Analysis of Immune cells

Published on: May 19, 2020

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
08:47

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Acute injury triggers inflammation, a key pathological process.
  • Inflammation involves inflammatory cytokines and adhesion molecules on cell surfaces.
  • Adhesion molecule cascades are implicated in neurological injury.

Purpose of the Study:

  • To review the role of adhesion molecules in secondary injury after cerebral ischemia and trauma.
  • To discuss potential therapeutic targets within the adhesion cascade.

Main Methods:

  • Literature review of basic science and clinical trials.
  • Focus on the mechanisms of adhesion molecules in neurological injury.

Main Results:

  • Adhesion molecules play a critical role in the development of secondary injury.
  • The adhesion cascade is a significant contributor to post-injury pathology.

Conclusions:

  • Understanding adhesion molecule function is crucial for managing neurological injury.
  • Targeting the adhesion cascade presents promising therapeutic avenues.