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Related Concept Videos

Inflammation01:38

Inflammation

Overview
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,...
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...
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 II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
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...

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Related Experiment Video

Updated: Jun 4, 2026

Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses
06:43

Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses

Published on: March 29, 2017

Ion channels in inflammation.

Michael Eisenhut1, Helen Wallace

  • 1Luton & Dunstable Hospital NHS Foundation Trust, Lewsey Road, Luton, UK. michael_eisenhut@yahoo.com

Pflugers Archiv : European Journal of Physiology
|February 1, 2011
PubMed
Summary
This summary is machine-generated.

Inflammation alters ion channel function, leading to physical illness and pain. Targeting these ion transport systems directly offers a localized therapeutic approach for inflammatory diseases.

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Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Related Experiment Videos

Last Updated: Jun 4, 2026

Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses
06:43

Increased Recovery Time and Decreased LPS Administration to Study the Vagus Nerve Stimulation Mechanisms in Limited Inflammatory Responses

Published on: March 29, 2017

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response
12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

Area of Science:

  • Physiology
  • Molecular Biology
  • Pathology

Background:

  • Inflammation is a common factor in vertebrate physical illnesses, causing fluid shifts, muscle dysfunction, and pain.
  • These pathological processes are linked to alterations in the number or function of ion channels.
  • Ion channel dysregulation is observed in various conditions, including diarrheal illnesses, pyelonephritis, allergies, acute lung injury, and septic shock.

Purpose of the Study:

  • To elucidate the role of ion channels in inflammation-induced diseases.
  • To identify the molecular mechanisms by which inflammatory mediators affect ion transport.
  • To propose targeted therapeutic strategies for inflammation.

Main Methods:

  • Review of existing literature on inflammation, ion channels, and related signaling pathways.
  • Analysis of how inflammatory mediators (cytokines, prostaglandins, reactive oxygen species, etc.) influence ion channel expression and function.
  • Examination of signaling cascades (cAMP, phosphoinositide, MAPK) involved in ion channel modulation during inflammation.

Main Results:

  • Inflammation significantly impacts all major ion channel categories (sodium, chloride, calcium, potassium, TRP, purinergic, ASICs).
  • Inflammatory mediators directly or indirectly alter ion channel activity through various signaling pathways and direct modifications.
  • Inflammation-induced pain is a direct consequence of altered ion transport.

Conclusions:

  • Ion channel dysfunction is a critical mechanism underlying inflammation-related diseases.
  • Therapeutic strategies should focus on directly and locally modulating the affected ion transport systems to mitigate adverse effects of inflammatory mediators.