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The cell biology of acute itch

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ABSTRACT

Itch, the irritation we feel and the relief that comes from scratching, is an evolutionary warning system and defense against harmful environmental agents. Although once considered a subtype of pain, itch is now recognized as a unique sense, with its own distinct physiology and cell receptors. Here, we discuss recent advances in our understanding of itch and the molecular players that mediate this sensory modality.

No MeSH data available.


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Multiple cell types contribute to peripheral itch. Prurinergic stimuli, here a mosquito bite, generates itch via the interaction of a variety of cell types. Keratinocytes release endogenous pruritogens, including thymic stromal lymphopoietin (TSLP), contributing directly to itch sensation by activating the TSLP receptor (TSLPR) on peripheral afferent neurons (Wilson et al., 2013). Keratinocytes also release chemoattractants that recruit immune cells, including mast cells. Histamine released from stored granules in mast cells binds H1 receptors, activating pruriceptors and transmitting itch signals to the spinal cord. Along with histamine, other pruritogens, including serotonin, proteases, and IL-6, are released by resident immune cells such as T cells and dendritic cells (Schmelz et al., 2003). The blue squares at the nerve endings represent the receptor for itchy substances.
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fig1: Multiple cell types contribute to peripheral itch. Prurinergic stimuli, here a mosquito bite, generates itch via the interaction of a variety of cell types. Keratinocytes release endogenous pruritogens, including thymic stromal lymphopoietin (TSLP), contributing directly to itch sensation by activating the TSLP receptor (TSLPR) on peripheral afferent neurons (Wilson et al., 2013). Keratinocytes also release chemoattractants that recruit immune cells, including mast cells. Histamine released from stored granules in mast cells binds H1 receptors, activating pruriceptors and transmitting itch signals to the spinal cord. Along with histamine, other pruritogens, including serotonin, proteases, and IL-6, are released by resident immune cells such as T cells and dendritic cells (Schmelz et al., 2003). The blue squares at the nerve endings represent the receptor for itchy substances.

Mentions: As the primary cell type found in skin, keratinocytes are capable of producing a variety of defenses against pathogens. In response to noxious stimuli, keratinocytes can release a host of inflammatory mediators, including nerve growth factor, IL-6, and serotonin, sensitizing peripheral neurons (Luo et al., 2015). Keratinocytes have also been shown to directly activate neurons via the release of the cytokine thymic stromal lymphopoietin, triggering itch behavior (Fig. 1; Wilson et al., 2013). Keratinocytes interact with the immune system via the release of chemoattractants, such as monocyte chemoattractant protein 1, chemokine ligand 5, and IL-8, recruiting immune cells to the site of injury or pruritinergic stimuli. These chemokines were found to be elevated in patients with atopic dermatitis and psoriasis, implicating keratinocytes in the pathology of itch (Giustizieri et al., 2001).


The cell biology of acute itch
Multiple cell types contribute to peripheral itch. Prurinergic stimuli, here a mosquito bite, generates itch via the interaction of a variety of cell types. Keratinocytes release endogenous pruritogens, including thymic stromal lymphopoietin (TSLP), contributing directly to itch sensation by activating the TSLP receptor (TSLPR) on peripheral afferent neurons (Wilson et al., 2013). Keratinocytes also release chemoattractants that recruit immune cells, including mast cells. Histamine released from stored granules in mast cells binds H1 receptors, activating pruriceptors and transmitting itch signals to the spinal cord. Along with histamine, other pruritogens, including serotonin, proteases, and IL-6, are released by resident immune cells such as T cells and dendritic cells (Schmelz et al., 2003). The blue squares at the nerve endings represent the receptor for itchy substances.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4862869&req=5

fig1: Multiple cell types contribute to peripheral itch. Prurinergic stimuli, here a mosquito bite, generates itch via the interaction of a variety of cell types. Keratinocytes release endogenous pruritogens, including thymic stromal lymphopoietin (TSLP), contributing directly to itch sensation by activating the TSLP receptor (TSLPR) on peripheral afferent neurons (Wilson et al., 2013). Keratinocytes also release chemoattractants that recruit immune cells, including mast cells. Histamine released from stored granules in mast cells binds H1 receptors, activating pruriceptors and transmitting itch signals to the spinal cord. Along with histamine, other pruritogens, including serotonin, proteases, and IL-6, are released by resident immune cells such as T cells and dendritic cells (Schmelz et al., 2003). The blue squares at the nerve endings represent the receptor for itchy substances.
Mentions: As the primary cell type found in skin, keratinocytes are capable of producing a variety of defenses against pathogens. In response to noxious stimuli, keratinocytes can release a host of inflammatory mediators, including nerve growth factor, IL-6, and serotonin, sensitizing peripheral neurons (Luo et al., 2015). Keratinocytes have also been shown to directly activate neurons via the release of the cytokine thymic stromal lymphopoietin, triggering itch behavior (Fig. 1; Wilson et al., 2013). Keratinocytes interact with the immune system via the release of chemoattractants, such as monocyte chemoattractant protein 1, chemokine ligand 5, and IL-8, recruiting immune cells to the site of injury or pruritinergic stimuli. These chemokines were found to be elevated in patients with atopic dermatitis and psoriasis, implicating keratinocytes in the pathology of itch (Giustizieri et al., 2001).

View Article: PubMed Central - HTML - PubMed

ABSTRACT

Itch, the irritation we feel and the relief that comes from scratching, is an evolutionary warning system and defense against harmful environmental agents. Although once considered a subtype of pain, itch is now recognized as a unique sense, with its own distinct physiology and cell receptors. Here, we discuss recent advances in our understanding of itch and the molecular players that mediate this sensory modality.

No MeSH data available.


Related in: MedlinePlus