Related Experiment Video
Updated: Apr 24, 2026
07:22
Basophil Activation Test for Allergy Diagnosis
Published on: May 31, 2021
9.9K
Histamine H4 receptor in oral lichen planus
A Salem1, A Al-Samadi, V Stegajev
1Department of Medicine, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland; Department of Oral Pathology, University of Helsinki, Helsinki, Finland.
Oral Diseases
|September 11, 2014
Summary
In oral lichen planus (OLP), histamine H4 receptors (H4Rs) on oral epithelial cells are reduced, linked to increased mast cells. This suggests H4Rs are vital for oral mucosa health, potentially impaired in OLP.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Oral lichen planus (OLP) is an autoimmune condition affecting oral mucosa.
- It involves T-cell infiltration, epithelial cell apoptosis, and basement membrane damage.
- Histamine H4 receptors (H4Rs) are implicated in immune responses.
Purpose of the Study:
- To investigate the hypothesis that H4Rs are downregulated in OLP.
- To determine the role of histamine and cytokines in H4R regulation in OLP.
Main Methods:
- Immunohistochemistry and immunofluorescence staining of OLP tissues.
- Quantitative real-time PCR on tissue samples and cultured oral keratinocytes.
- Analysis of mast cell (MC) counts and H4R immunoreactivity.
Main Results:
- H4R immunoreactivity was significantly weaker in OLP tissues compared to controls.
- Weak H4R staining in OLP correlated negatively with mast cell hyperplasia and degranulation.
- High histamine concentrations and interferon-γ reduced H4R gene expression, while H4R agonists caused rapid receptor internalization.
Conclusions:
- Healthy oral epithelium expresses H4Rs independently of mast cells.
- In OLP, increased activated mast cells are associated with decreased epithelial H4R expression.
- H4R dysfunction, driven by mast cell degranulation and cytokines, may impair oral mucosa maintenance in OLP.
Related Concept Videos
01:28Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists
1.3K
Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
1.3K
01:30Hypersensitivities
7.2K
Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
7.2K
01:29Hypersensitivity Reactions: Delayed Hypersensitivity Reactions
343
Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
343
01:22Pathophysiology of Peptic Ulcer Disease: Injurious Factors
1.6K
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...
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...
1.6K
01:26Gastritis II: Pathophysiology
33
The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
33
01:30Allergic Reactions: Anaphylaxis
267
Anaphylaxis is a severe, life-threatening hypersensitivity reaction mediated by Immunoglobulin E (IgE) antibodies. When IgE binds to allergens, it triggers the release of mediators– histamine, leukotrienes, and prostaglandins from mast cells and basophils. These mediators cause vasodilation, edema, and inflammation, leading to various symptoms.The primary allergens causing anaphylaxis include food items (e.g., peanuts, shellfish), drugs (e.g., penicillin, asparaginase, corticotropin,...
267