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

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

494
Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
494
Accessory Structures of the Skin: Sebaceous Glands01:21

Accessory Structures of the Skin: Sebaceous Glands

2.0K
A sebaceous gland is a type of oil gland found almost all over the skin ( except palms and soles) and helps lubricate and waterproof the skin and hair. Most sebaceous glands are associated with hair follicles. They generate and excrete sebum, a mixture of lipids, onto the skin surface, thereby naturally lubricating the dry and dead layer of keratinized cells of the stratum corneum, keeping it pliable.
These glands that produce the oils on the skin and hair are holocrine glands. The mature...
2.0K
Skin Diseases and Disorders01:23

Skin Diseases and Disorders

4.0K
Skin is the first line of defense and encounters a variety of microbes. Some pathogenic strains are often the cause of a broad range of infections of the skin and other body systems. These conditions can affect people of all ages and may have different causes, including genetic factors, infections, autoimmune reactions, environmental factors, and lifestyle choices.
Gram-positive Staphylococcus spp. and Streptococcus spp. are responsible for many of the most common skin infections. However, many...
4.0K
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

645
Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
645
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

671
Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
671
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

244
Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...
244

You might also read

Related Articles

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

Sort by
Same author

Single-cell transcriptome reveals keratinocyte subclusters contributing to altered differentiation and inflammatory responses in atopic dermatitis.

Nature communications·2026
Same author

ADAR1 loss-of-function variants altering RNA editing define a new interferon-dependent psoriasis subtype.

The Journal of experimental medicine·2026
Same author

A single-cell atlas identifies oncogenic transcriptional programs and immune escape mechanisms in CTCL.

Blood·2026
Same author

Hailey-Hailey disease models identify synergistic therapeutic effects of MEK and ROCK inhibition.

bioRxiv : the preprint server for biology·2026
Same author

A longitudinal atlas of human psoriatic skin reveals the mechanisms of anti-IL-23 therapy in disrupting the type 17 inflammatory circuit.

Immunity·2026
Same author

Multicytokine-based transcriptome-wide association study for 7 inflammatory skin disorders identifies candidate causal genes in keratinocytes.

The Journal of allergy and clinical immunology·2026

Related Experiment Video

Updated: Aug 10, 2025

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

39.0K

Pathophysiology of generalized pustular psoriasis.

Kelly Z Young1, Mrinal K Sarkar2, Johann E Gudjonsson2

  • 1University of Michigan Medical School, Ann Arbor, Michigan, USA.

Experimental Dermatology
|February 13, 2023
PubMed
Summary

Generalized pustular psoriasis, a severe skin condition, involves autoinflammatory responses. Research highlights the IL-36 immune axis

Keywords:
IL-36autoinflammationgeneralized pustular psoriasisgeneticspsoriasis vulgaris

More Related Videos

Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.6K
Author Spotlight: Self-Assessment Protocol for Predicting Psoriatic Arthritis in Psoriasis Patients
02:28

Author Spotlight: Self-Assessment Protocol for Predicting Psoriatic Arthritis in Psoriasis Patients

Published on: March 1, 2024

474

Related Experiment Videos

Last Updated: Aug 10, 2025

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
11:39

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis

Published on: July 11, 2013

39.0K
Granulocyte-dependent Autoantibody-induced Skin Blistering
12:23

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

10.6K
Author Spotlight: Self-Assessment Protocol for Predicting Psoriatic Arthritis in Psoriasis Patients
02:28

Author Spotlight: Self-Assessment Protocol for Predicting Psoriatic Arthritis in Psoriasis Patients

Published on: March 1, 2024

474

Area of Science:

  • Immunodermatology
  • Genetics
  • Autoinflammatory Diseases

Background:

  • Psoriasis is a prevalent chronic skin disease affecting over 3% of US adults.
  • Generalized pustular psoriasis (GPP) is a severe subtype with high morbidity and mortality.
  • GPP pathogenesis involves autoinflammatory pathways, distinct from plaque psoriasis' adaptive immune dysregulation.

Purpose of the Study:

  • To review psoriatic subtypes and GPP diagnostic criteria.
  • To discuss newly identified genetic variants in pustular psoriasis.
  • To elucidate the role of the IL-36 immune axis in GPP.

Main Methods:

  • Review of psoriatic subtypes and GPP diagnostic criteria.
  • Analysis of genetic variants associated with pustular psoriasis.
  • Integration of transcriptomic data to understand IL-36 pathway involvement.

Main Results:

  • Recent genetic studies identified novel variants linked to pustular skin disease.
  • Transcriptomic studies confirm the pathogenic role of the IL-36 immune axis in GPP.
  • Understanding genetic variants sheds light on pustular disease mechanisms.

Conclusions:

  • The IL-36 immune axis is a critical factor in generalized pustular psoriasis development.
  • Genetic and transcriptomic insights advance understanding of GPP pathogenesis.
  • Further research into the IL-36 pathway may reveal new therapeutic targets for GPP.