Mast cell–driven skin inflammation is impaired in the absence of sensory nerves

Siebenhaar, Frank; Magerl, Markus; Peters, Eva M.J.; Hendrix, Sven; Metz, Martin; Maurer, Marcus

doi:10.1016/j.jaci.2007.11.013

Cited by 77 publications

(56 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Topical capsaicin induces dermal mast cell degranulation in adults mainly via tachykinin release from sensory C-fibers (9,16,26). However, in this study, capsaicin had no such effect in pups, although the number of dermal mast cells per 1 mm 2 of skin was higher in pups than in adults.…”

Section: Discussioncontrasting

confidence: 75%

“…The age-dependent difference in mast cell degranulation may be closely associated with the age difference in releasability of tachykinins from sensory C-fibers. The secondary release of histamine and serotonin from mast cells causes plasma leakage in the skin (9,16,26). Therefore, the age-dependent difference in neurogenic-mediated skin plasma leakage may be partly because of the age-related difference in mast cell degranulation via a neurogenic-mediated pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Degranulating mast cells were histomorphologically distinguished from intact nondegranulating cells as previously described (Ͼ10% of the cytoplasmic granules exhibiting fusion, stain alterations, or extrusion from the cells; Refs. 15,16).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Development of Mechanisms Associated With Neurogenic-Mediated Skin Inflammation During the Growthof Rats

et al. 2010

View full text Add to dashboard Cite

Neurogenic-mediated inflammation may be associated with several inflammatory skin diseases including atopic dermatitis. However, age-dependent differences in neurogenic-mediated skin responses are not fully understood. We compared skin plasma leakage in rats aged 2 and 8 wk, which was induced by topical capsaicin, topical formalin, and intracutaneous substance P, whose effects are mediated via tachykinin NK1 receptors. Evans blue dye extravasation served as an index of the increase in skin vascular permeability. Capsaicin, formalin, and substance P caused a skin response in a dose-dependent manner in both age groups. However, the skin response was much greater in adults than in pups. In addition, the localization of sensory C-fibers and tachykinin NK1 receptors in the skin was investigated by immunofluorescent staining with antisubstance P and antitachykinin NK1 receptor antibodies, respectively. Substance P-immunoreactive nerves were detected throughout the dermis and tachykinin NK1 receptors were mainly detected in blood vessel walls in the dermis in both age groups. However, they were more sparsely distributed in pups. In conclusion, the weak neurogenic-mediated skin inflammation in pups is probably because of immature neural mechanisms associated with skin inflammation such as reduced innervation of sensory C-fibers and low expression of tachykinin NK1 receptors. (Pediatr Res 67: 363-368, 2010) N eurogenic-mediated inflammation may be associated with several inflammatory skin diseases including atopic dermatitis (1). Immediately after stimulation of nerve endings of sensory C-fibers, antidromic conduction through afferent nerve collaterals causes the release of neuropeptides such as substance P and calcitonin gene-related peptide from nerve endings of sensory C-fibers. The released neuropeptides lead to pain, pruritus, vascular modulation (i.e. plasma leakage, vasodilation, and endothelial cell activation), and activation of immune cells including T-and B-cells, and mast cells (1-3).In animal experimental models, it is more difficult to elicit neurogenic-mediated skin inflammation in younger animals, particularly during the perinatal period. Fitzgerald and Gibson (4) showed that topical mustard oil and antidromic stimulation of the sciatic nerve of rats, which specifically stimulate sensory C-fibers in the skin, are incapable of producing plasma leakage in the paw until postnatal day 11. However, this is inconsistent with previous data that substance P-immunoreactive nerves are detected even in the skin of rats aged day 0 -1 (4,5). Schotzinger and Landis (5) reported increases in the number of substance P-immunoreactive nerves in rat skin, branching pattern of nerves, and substance P immunoreactivity throughout neonatal life that approach adult levels by postnatal day 21. Therefore, the histologic immaturity of sensory C-fibers may be one reason for the lack or reduced level of neurogenic-mediated skin inflammation in rat pups. Neurogenic-mediated skin inflammation is also likely to depend on the e...

show abstract

Section: Discussioncontrasting

confidence: 75%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Development of Mechanisms Associated With Neurogenic-Mediated Skin Inflammation During the Growthof Rats

et al. 2010

View full text Add to dashboard Cite

show abstract

“…SP is known to provide a positive feedback on MCs by causing degranulation and the release of pro-inflammatory mediators that, in turn, can attract other inflammatory cells [31][32][33].…”

Section: Mast Cells In Ems: a Painful Liaison?mentioning

confidence: 99%

Mast cells in endometriosis: guilty or innocent bystanders?

Kirchhoff

Kaulfuß

Fuhrmann

et al. 2012

Expert Opinion on Therapeutic Targets

Self Cite

View full text Add to dashboard Cite

“…Currently, Peters and coworkers demonstrated that stress worsens dermatitis via substance P-dependent neurogenic inflammation in mice (Pavlovic et al, 2007). Maurer and coworkers demonstrated that sensory skin nerves augment mast cell-driven inflammatory responses by releasing neuropeptides that increases mast cell degranulation in a mouse model of passive cutaneous anaphylaxis (Siebenhaar et al, 2008). Kurebayashi and coworkers attempted to generate 2,4,6-trinitrobenzene sulfonic acid-induced colitis in rats, and found that mast cell-deficient Ws/Ws rats did not manifest symptoms of visceral hypersensitivity in this model (Ohashi et al, 2008).…”

Section: Possible Implication Of Cadm1-mediated Nerve-mast Cell Intermentioning

confidence: 99%

Nerve-mast cell and smooth muscle-mast cell interaction mediated by cell adhesion molecule-1, CADM1

Ito

Hagiyama

Oonuma

2008

J. Smooth Muscle Res.

View full text Add to dashboard Cite

Mast cells are a native composer of connective tissue of the skin dermis and intestinal and respiratory mucosa. Independent lines of accumulated evidence indicate the existence of an intensive bidirectional crosstalk between mast cells and sensory nerves and suggest that mast cells and sensory nerves may be viewed as a functional unit, which could be of crucial importance in neuroimmunological pathways. Mast cells appear to have a property of influencing smooth muscle function via not only such nerve-mast cell effects, but also direct pathways. In bronchial asthma, mast cells infiltrate the airway smooth muscle layer, and interact directly with smooth muscle cells, suggesting pathogenic roles for mast cells in airway obstruction. Current studies on mast cell biology identified a novel adhesion molecule of mast cells, namely cell adhesion molecule-1, CADM1. This molecule is unique, because it serves as not only simple glue but also appears to promote functional communication between nerve and mast cells and between smooth muscle and mast cells.

show abstract

Mast cell–driven skin inflammation is impaired in the absence of sensory nerves

Cited by 77 publications

References 73 publications

Development of Mechanisms Associated With Neurogenic-Mediated Skin Inflammation During the Growthof Rats

Development of Mechanisms Associated With Neurogenic-Mediated Skin Inflammation During the Growthof Rats

Mast cells in endometriosis: guilty or innocent bystanders?

Nerve-mast cell and smooth muscle-mast cell interaction mediated by cell adhesion molecule-1, CADM1

Contact Info

Product

Resources

About