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Related Concept Videos

Inflammation: Introduction01:28

Inflammation: Introduction

Inflammation is a fundamental, protective biological response of vascularized tissues to cellular injury, infection, or harmful stimuli. Its primary function is to eliminate the initial cause of injury, clear necrotic cells and damaged tissue, and initiate the necessary repair processes.Cardinal SignsAcute inflammation presents with classic signs. Redness results from vasodilation and increased blood flow. Heat is due to increased metabolism and circulation. Swelling results from the...
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,...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Inflammation

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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...
Pigmentation01:19

Pigmentation

The color of the skin is influenced by a number of pigments, including melanin, carotene, and hemoglobin. Recall that melanin is produced by cells called melanocytes, which are found scattered throughout the stratum basale of the epidermis. The melanin is transferred to the keratinocytes via melanosomes.
Melanin occurs in two primary forms: eumelanin that provides black and brown pigment and pheomelanin that provides red color. Dark-skinned individuals produce more melanin than those with pale...

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Related Experiment Video

Updated: Jul 9, 2026

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages
06:52

Detection of Inflammasome Activation and Pyroptotic Cell Death in Murine Bone Marrow-derived Macrophages

Published on: May 21, 2018

Sunburned skin activates inflammasomes.

Benjamin Faustin1, John C Reed

  • 1Burnham Institute for Medical Research, La Jolla, CA 92037, USA.

Trends in Cell Biology
|December 18, 2007
PubMed
Summary

Ultraviolet (UV) irradiation causes skin inflammation by activating caspase-1 in keratinocytes. Recent findings reveal that NOD-like receptors (NLRs) act as key intermediaries in this UV-induced inflammasome activation pathway.

Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Ultraviolet (UV) irradiation is a known cause of skin injury, leading to sunburn and inflammation.
  • UV-irradiated keratinocytes release interleukin-1beta via a caspase-1-dependent pathway.
  • The precise mechanism linking UV exposure to caspase-1 activation has been an area of investigation.

Purpose of the Study:

  • To investigate the role of NOD-like receptors (NLRs) in the UV-induced inflammatory response.
  • To elucidate the link between UV irradiation and caspase-1 activation in skin cells.
  • To understand how cell injury from UV light triggers innate immune pathways.

Main Methods:

  • The study focused on the cellular mechanisms following UV irradiation.
  • Investigated the involvement of inflammasome components, specifically NLRs and caspase-1.

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Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
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  • Examined the secretion of inflammatory mediators like interleukin-1beta from keratinocytes.

    • Main Results:

    • UV-irradiated keratinocytes activate caspase-1, leading to inflammation.
    • NOD-like receptors (NLRs) play a significant role in mediating UV-induced caspase-1 activation.
    • NLRs function by assembling inflammasomes, which are crucial for caspase activation.

    Conclusions:

    • NLRs are identified as critical intermediaries connecting UV-induced cell injury to inflammation.
    • The findings highlight the inflammasome pathway's involvement in the skin's response to UV radiation.
    • Further research into UV-induced inflammasome activation can inform strategies for managing skin inflammation.