Expression of IL-31 gene transcripts in NC/Nga mice with atopic dermatitis

Takaoka, Akiko; Arai, Iwao; Sugimoto, Masako; Yamaguchi, Akie; Tanaka, Makoto; Nakaike, Shiro

doi:10.1016/j.ejphar.2005.04.040

Cited by 114 publications

(76 citation statements)

References 7 publications

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“…As in the case of IL-13, transgenic overexpression of IL-31 also induced severe pruritus and dermatitis in mice [144]. Further supporting its role, increased expression of IL-31 was found both in an atopic mouse model [145] and in AD patients [146,147] in good correlation with the scratching behavior in mice [148] and the symptom severity in humans [149,150]. The exact pruritogenic mechanism of action of IL-31 is still unclear although IL-31 receptors were detected on a fraction of small diameter sensory neurons [151] as well as on normal human epidermal keratinocytes (NHEKs) [152].…”

Section: Inflammatory Mediators As Peripheral Itch Sensitizerssupporting

confidence: 54%

TRP Channels and Pruritus

Tóth¹,

Bı́ró²

2013

TOPAINJ

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Itch (pruritus) is one of the most often seen sensory phenomena in clinical practice. Recent neurophysiological findings proposed the existence of a novel pruriceptive system which includes a multitude of pruritogenic (itch-inducing) peripheral mediators, itch-selective pruriceptors, sensory afferent networks, spinal cord neurons, and certain central nervous system regions. In this review, we first introduce major features of the pruriceptive system. We then focus on defining the roles of transient receptor potential (TRP) ion channels in skin-coupled itch and provide compelling evidence that certain thermosensitive TRP channels (especially TRPV1, TRPV3, TRPV4, and TRPA1) are indeed key players in pruritus pathogenesis. Finally, we propose TRP-centered future experimental directions towards the therapeutic targeting of TRP channels in the clinical management of itch.

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Section: Inflammatory Mediators As Peripheral Itch Sensitizerssupporting

confidence: 54%

TRP Channels and Pruritus

Tóth¹,

Bı́ró²

2013

TOPAINJ

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“…Investigation of IL-31 transgenic mice showed that overexpression of IL-31 resulted in the development of AD-like lesions, and that IL-31 expression was highly associated with Th2-skewed T cells (1). In a nontransgenic murine model of spontaneous AD development, increased levels of IL-31 mRNA were associated with scratching behavior (24,25), and subsequent inhibition of scratching was achieved using a neutralizing anti-IL-31 mAb (15). Finally, increased levels of IL-31 mRNA have been associated with samples from human AD patients (2,5), and these IL-31 levels were further shown to correlate with increases in IL-4 and IL-13 (3).…”

Section: Discussionmentioning

confidence: 99%

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Bilsborough

Mudri²,

Chadwick³

et al. 2010

The Journal of Immunology

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IL-31 signals through the heterodimeric receptor IL-31RA and oncostatin M receptor (OSMR), and has been linked with the development of atopic dermatitis, a Th2 cytokine-associated disease in humans. However, recent studies of IL-31RA knockout (KO) mice have suggested that IL-31 signaling may be required to negatively regulate Th2 type responses rather than exacerbate them. Because those studies were performed on genetically modified mice, we examined whether neutralizing IL-31 with a specific mAb would give similar results to IL-31RA KO mice in two Th2 cytokine-associated immune models. We report no difference in lymphocyte Th2-type cytokine production after Ag immunization between IL-31RA KO mice, mice treated with the IL-31 mAb, or control animals. Second, we tested whether the absence of the IL-31RA subunit in IL-31RA KO mice may allow for increased pairing of the OSMR subunit with another cytokine receptor, gp130, resulting in overrepresentation of the heterodimeric receptor for OSM and increased responsiveness to OSM protein. We found that intranasal OSM challenge of IL-31RA KO mice resulted in increased IL-6 and vascular endothelial growth factor production in the lung compared with wild-type littermate control animals. Moreover, PBS-challenged IL-31RA KO mice already had increased levels of vascular endothelial growth factor, which were further increased by OSM challenge. These data imply that IL-31RA–deficient mice produce increased levels of OSM-inducible cytokines during airway sensitization and challenge, which may be the driving force behind the apparent exacerbation of Th2-type inflammatory responses previously observed in these mice.

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“…For example, IL-31 mRNA in the skin of NC/Nga mice (atopic dermatitis mouse model) with scratching behavior was found to be significantly higher than that in NC/Nga mice without scratching behaviour 19 .…”

Section: Interleukin 31 (Il-31)mentioning

confidence: 97%

“…The newly discovered interleukin, IL-31 might have a major role in pathophysiology of pruritus, especially in atopic dermatitis 19 . For example, IL-31 mRNA in the skin of NC/Nga mice (atopic dermatitis mouse model) with scratching behavior was found to be significantly higher than that in NC/Nga mice without scratching behaviour 19 .…”

Section: Interleukin 31 (Il-31)mentioning

confidence: 99%

Chronic Pruritus: Clinics and Treatment

Grundmann

Ständer

2011

Ann Dermatol

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Chronic pruritus, one of the main symptoms in dermatology, is often intractable and has a high impact on patient's quality of life. Beyond dermatologic disorders, chronic pruritus is associated with systemic, neurologic as well as psychologic diseases. The pathogenesis of acute and chronic (＞6 weeks duration) pruritus is complex and involves in the skin a network of resident (e.g., sensory neurons) and transient inflammatory cells (e.g., lymphocytes). In the skin, several classes of histamine-sensitive or histamine-insensitve C-fibers are involved in itch transmission. Specific receptors have been discovered on cutaneous and spinal neurons to be exclusively involved in the processing of pruritic signals.Chronic pruritus is notoriously difficult to treat. Newer insights into the underlying pathogenesis of pruritus have enabled novel treatment approaches that target the pruritusspecific pathophysiological mechanism. For example, neurokinin-1 antagonists have been found to relieve chronic pruritus. (Ann Dermatol 23(1) 1∼11, 2011)

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Expression of IL-31 gene transcripts in NC/Nga mice with atopic dermatitis

Cited by 114 publications

References 7 publications

TRP Channels and Pruritus

TRP Channels and Pruritus

IL-31 Receptor (IL-31RA) Knockout Mice Exhibit Elevated Responsiveness to Oncostatin M

Chronic Pruritus: Clinics and Treatment

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