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Inflammation

Inflammation

Formation of the Platelet Plug

Formation of the Platelet Plug

The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...

Inflammatory Response

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,...

Structure and Function of Platelets

Structure and Function of Platelets

The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000 platelets, with...

Acute Inflammation II: Cellular Phase

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...

Acute Inflammation III: Local and Systemic Effects

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...

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Related Experiment Video

Updated: Jun 2, 2026

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

Published on: September 27, 2019

Platelets Orchestrate a Neuroimmune Axis Driving Cutaneous Inflammation and Itch.

Ximin Hu^1,2,3, Fujun Wang^1,4, Ting Wang²

¹Department of Burn and Plastic Surgery, School of Medicine, the Second Affiliated Hospital of South China University of Technology (Guangzhou First People's Hospital), Guangzhou 510180, China.

Research (Washington, D.C.)

|June 1, 2026

Summary

Platelets drive skin inflammation and chronic itch by releasing serotonin, which activates immune cells and nerves. Targeting this platelet-immune-neuron axis offers a new therapeutic strategy for inflammatory skin diseases.

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Last Updated: Jun 2, 2026

Cheek Injection Model for Simultaneous Measurement of Pain and Itch-related Behaviors

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Published on: September 27, 2019

Cutaneous Surgical Denervation: A Method for Testing the Requirement for Nerves in Mouse Models of Skin Disease

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Published on: June 26, 2016

Granulocyte-dependent Autoantibody-induced Skin Blistering

Granulocyte-dependent Autoantibody-induced Skin Blistering

Published on: October 12, 2012

Area of Science:

Dermatology
Immunology
Neuroscience

Background:

Platelets are known for hemostasis but their role in skin neuroimmune signaling is unclear.
Investigating platelet function in skin inflammation and chronic itch is crucial.

Purpose of the Study:

To elucidate the functional contribution of platelets to skin inflammation and chronic itch.
To explore the platelet-immune-neuron axis in cutaneous disorders.

Main Methods:

Multi-modal genetic and pharmacological strategies were employed.
Optogenetic platelet activation and platelet depletion were used in experimental models.
Transcriptomic profiling and re-analysis of clinical datasets were performed.

Main Results:

Platelet activation induced skin inflammation, erythema, and itch, mirroring atopic dermatitis (AD).
Platelet depletion reduced scratching, inflammation, and C-fiber excitability in AD models.
Platelet-derived serotonin (5-HT) mediated vascular leakage, macrophage recruitment, and pruriceptor sensitization via HTR2B/HTR7 signaling.

Conclusions:

The platelet-immune-neuron axis is a key driver of skin inflammation and chronic itch.
Targeting serotonin receptors (HTR2B/HTR7) or platelets (e.g., clopidogrel) can attenuate inflammation and itch.
This axis represents a promising therapeutic target for inflammatory skin disorders.