ライフサイエンスコーパス: itch

1 ing chemical itch, also abolishes mechanical itch.

2 us agents that elicit or exacerbate pain and itch.

3 n-31, which acts on neurons to promote wound itch.

4 known ligands and receptors associated with itch.

5 lose to the skin contribute significantly to itch.

6 for converting innocuous touch to irritating itch.

7 tractive target for the treatment of chronic itch.

8 and uncover potential targets for combating itch.

9 on of macrophages deficient in the E3 ligase ITCH.

10 on and stress, and in turn, inhibit pain and itch.

11 racterize the role of NK1R spinal neurons in itch.

12 capsaicin-induced pain and histamine-induced itch.

13 ations such as temperature, touch, pain, and itch.

14 usters that regulate pain, inflammation, and itch.

15 re part of the circuit for pruritogen-evoked itch.

16 epidermal-neural mechanism of AD associated itch.

17 sly implicated in gating mechanical pain and itch.

18 omising strategy for alleviating cholestatic itch.

19 detect noxious stimuli, leading to pain and itch.

20 only report experiencing an intense, chronic itch.

21 t temporal patterns during acute and chronic itch.

22 rt experiencing an intense non-histaminergic itch.

23 strategy for alleviating jaundice-associated itch.

24 hotomy exists for the role of VTA in chronic itch.

25 eurons, may encode the aversive component of itch.

26 odifying treatment for atopic dermatitis and itch.

27 dly useful for the study of touch, pain, and itch.

28 hat that CXCR3 antagonism attenuates chronic itch.

29 ant for mediating the affective component of itch.

30 cing enzyme biliverdin reductase, attenuates itch.

31 eception, mechanoreception, nociception, and itch.

32 y and affective aspects of acute and chronic itch.

33 lectively required for AD-associated chronic itch.

34 ic itch, without impairing histamine-induced itch.

35 skin tests and as an inducer of experimental itch.

36 logy and therapeutic development for chronic itch.

37 ral responses in multiple models of pain and itch.

38 by recurrent eczematous lesions and intense itch.

39 voked persistent pain and pruritogen-induced itch.

40 l circuitry responsible for the sensation of itch.

41 xis with implications for treatment of wound itching.

42 s leading to plasma extravasation, pain, and itching.

43 rses suggested Na(V)1.8 to sustain prolonged itching.

44 associated with the unpleasant sensation of itching.

45 h is regulated by itchy E3 ubiquitin ligase (ITCH), a negative regulator of inflammation.

46 plays pronounced deficit in chronic dry skin itch, a type of chemical itch in mice.

47 Mixed bone marrow chimeras revealed that Itch acts within B cells to limit naive and, to a greate

48 ic itch patients, the affective component of itch affects both quality of life (leading to psychologi

49 were also effective in decreasing psoriatic itch after the repeated application of imiquimod, which

50 Paradoxically, scratching the itch also produces a hedonic experience.

51 hich are essential for transmitting chemical itch, also abolishes mechanical itch.

52 ed and assessed in 137 patients with chronic itch and atopic dermatitis or psoriasis.

53 um anticytokine therapeutics for controlling itch and atopic skin inflammation.

54 antly reversed imiquimod-established chronic itch and cutaneous inflammation.

55 t to suggest a role for NK1R interneurons in itch and extend our understanding of the complexities of

56 t to suggest a role for NK1R interneurons in itch and extends our understanding of the complexities o

57 -nerve interactions play an integral role in itch and inflammation.

58 deoxycholic acid (UDCA) treatment can reduce itch and lower endogenous serum bile acids in intrahepat

59 We aimed to analyze the association between itch and mental health in dermatological patients.

60 ctivated TRPV1(+) sensory neurons leading to itch and pain behaviors.

61 isms by which inflammatory cytokines promote itch and pain sensations to coordinate host-protective b

62 y contrast, capsaicin, which evokes a mix of itch and pain sensations, enhances both excitatory and i

63 Sensitization of mechanical itch and persistent spontaneous itch are intractable sym

64 ur data not only expand our understanding of itch and psoriasis, but also reveal TRPC4 as a potential

65 The Sleep-Related Itch and Scratch Scale consisted of one factor that acco

66 interactions that trigger the development of itch and the acute-to-chronic itch transition remain unk

67 eds new light on the neural basis of chronic itch and unveils novel avenues for developing mechanism-

68 Median itch and VSS scores were highest for GG homozygotes and

69 ary outcomes included additional measures of itching and disease severity.

70 itis, are clinically characterized by severe itching and type 2 immunity-associated hypersensitivity

71 yping of the TRPA1 KO rat in models of pain, itch, and asthma that have previously only been investig

72 species for pharmacological studies in pain, itch, and asthma, but until recently, genetic manipulati

73 enable more sophisticated modeling of pain, itch, and asthma.

74 urons play a fundamental role, such as pain, itch, and asthma.

75 ide in sensory neurons for non-histaminergic itch, and GRP sensory neurons are dedicated to itch tran

76 d is a therapeutic target for treating pain, itch, and respiratory diseases.

77 use, key VKC symptoms (photophobia, tearing, itching, and mucous discharge), and quality of life (QoL

78 ce, the molecular and cellular mechanisms of itch are being intensely studied.

79 Pain, temperature, and itch are conventionally thought to be exclusively transd

80 f mechanical itch and persistent spontaneous itch are intractable symptoms in chronic itch patients.

81 herapeutics that specifically target chronic itch as a pathologic entity are currently still not avai

82 new light on the pathophysiology of pain and itch as well as the physiology of touch.

83 Their findings link itch associated with deeper wounds-wounds that extend be

84 eutic modalities available for SD-associated itch because little is known about its pathophysiologica

85 ental neuroimmune axis in the development of itch because of the traditional prominence of histamine

86 ion of Tacr1(CreER) spinal neurons increases itch behavior in male and female mice, whereas pharmacol

87 nin-1 receptor (NK1R) spinal neurons mediate itch behavior in mice and that the majority of NK1R spin

88 Here, we investigated contagious itch behavior in the mouse model of fragile X syndrome (

89 study has shown that mice exhibit contagious itch behavior while viewing a scratching demonstrator mo

90 se model of FXS shows deficits in contagious itch behavior.

91 logical inhibition of spinal NK1R suppresses itch behavior.

92 ced pain behavior was increased, whereas the itching behavior was unchanged in CCI models compared wi

93 ew aims to introduce these basic concepts in itch biology and highlight how distinct immunologic path

94 and function of the mast cell-nerve unit in itch biology.

95 y, the mutants have increased sensitivity to itch, but acute sensitivity to other sensory stimuli suc

96 as a neurotransmitter for non-histaminergic itch, but its site of action (sensory neurons vs spinal

97 geneics and chemogenetics in the skin evokes itch- but not pain-related scratching or wiping behavior

98 AR) agonist, relieves cholestasis-associated itch by alleviating hepatobiliary injury.

99 1.9 were compared for their contribution to itch by analysing Na(V)-specific knockout mice.

100 Itch can be a behavioral extension of type 2 immunity by

101 PZ-235 significantly reduced itching caused by wasp venom peptide degranulation of ma

102 Recent seminal advances in itch circuitry within the nervous system have intersecte

103 understanding of the complexities of spinal itch circuitry.

104 rther dissection of their function in spinal itch circuitry.

105 understanding of the complexities of spinal itch circuitry.SIGNIFICANCE STATEMENT The spinal cord is

106 (standard deviation = 15.7) in controls with itch compared with 82.9 (standard deviation = 15.6) in c

107 (standard deviation = 20.1) in patients with itch, compared with 74.7 (standard deviation = 18.0) in

108 mong sleep, itching, scratching, and chronic itch conditions and their associations with disease seve

109 Itch contributes substantially to the psychological dise

110 The neural substrate for touch-to-itch conversion in the spinal cord remains elusive.

111 Our data suggest that ITCH could be silenced both in vitro and in vivo using n

112 The ITCH-deficient macrophages had increased levels of the m

113 lammatory macrophages, which was enhanced in ITCH-deficient macrophages.

114 enuated pro-inflammatory polarization of the ITCH-deficient macrophages.

115 While Itch-deficient mice displayed normal numbers of preimmun

116 Chronic itch, defined as itch lasting longer than 6 weeks, is a

117 Itch did not demonstrate a statistically significant dif

118 We now show that Itch directly limits B cell activity.

119 Most chronic itch diseases are thought to be driven by both the nervo

120 s appreciated increasingly that most chronic itch disorders are likely nonhistaminergic in nature, pr

121 ffective targeted therapies for some chronic itch disorders such as atopic dermatitis has given wides

122 Thus, cDC2s promote itching during skin would healing via a TGF-beta-IL-31 a

123 mouse with targeted expression of MRGPRX4 in itch-encoding sensory neurons.

124 rain, circuits that mediate touch, pain, and itch engage in cross modulation.

125 eutrophil depletion significantly attenuated itch-evoked scratching in a mouse model of atopic dermat

126 B cells lacking Itch exhibited increased proliferation, glycolytic capac

127 ith ITCH siRNA could effectively silence the ITCH expression, and result in the stabilization of TP73

128 gated the mechanisms underlying this type of itch, focusing on the contribution of soluble factors re

129 we dissected a neural circuit for prolonged itch formed as Grpr(+) neurons act downstream of Npr1(+)

130 re that was further reflected in more severe itching, frequent flares, and increased disease severity

131 Intractable or recurrent chronic itch greatly reduces the patients' QOL and impairs their

132 AKT activation of ITCH-H1.2 axis may confer TNBC cells with a DDR repressi

133 Although the medical definition of itch has been in existence for 360 years, only in the la

134 endogenous mechanisms for reducing pain and itch holds enormous potential for developing new treatme

135 (scores range from 0 [no itch] to 10 [worst itch imaginable]).

136 spinal mechanisms responsible for prolonged itch in a mouse model of allergic contact dermatitis ind

137 and is known to suppress mechanical pain and itch in adults.

138 mast cell activation through MRGPRB2 drives itch in allergic contact dermatitis.

139 o contribute to lesion formation and intense itch in atopic dermatitis.

140 t immune cells that enter the skin and cause itch in atopic dermatitis.

141 d recognition to the importance of measuring itch in clinical trials.

142 oking some skin regions can evoke mechanical itch in healthy human subjects.

143 These results support a novel role for Itch in limiting B cell metabolism and proliferation to

144 ivation via Mrgprb2 evoked non-histaminergic itch in mice independently of the IgE-Fc epsilon RI (Fce

145 investigated the neuronal basis of affective itch in mice, with a focus on the amygdala, the key brai

146 in chronic dry skin itch, a type of chemical itch in mice.

147 Mrgprb2 deficiency decreased itch in multiple preclinical models of allergic contact

148 nificant association between the presence of itch in patients and clinical depression (odds ratio, 1.

149 rn neurons and has been suggested to mediate itch in rodents.

150 e, we sought to investigate the mediators of itch in SD using an immunofluorescence study on patient

151 The presence of itch in SD was significantly associated with the amount

152 IL-31 from macrophages may play a role in itch in SD.

153 f the recently identified peptides mediating itch in the spinal cord.

154 e inhibitors significantly inhibited chronic itch in these models.

155 ated from hyperbilirubinemic patients evoked itch in wild-type animals but not Mrgpra1(-/-) animals.

156 s into healthy skin was sufficient to induce itching in a manner dependent on IL-31 expression.

157 vior.SIGNIFICANCE STATEMENT The sensation of itch includes an affective component that leads to stres

158 the receptors of different neuropeptides for itch, including gastrin-releasing peptide receptor, natr

159 gs indicate that KLK7 promotes AD-associated itch independently from skin inflammation and reveal a p

160 eptidergic DRG neurons and showed that acute itch induced by serotonin and histamine was attenuated i

161 Laminae I/II INs drive chemical itch-induced scratching, laminae II/III INs generate paw

162 Itch, inflammation, and atopic dermatitis are associated

163 en TRPV3 and PAR2 in keratinocytes to convey itch information and suggest that a blockade of PAR2 or

164 ts suggest that innocuous touch and chemical itch information converge on GRPR neurons and thus map a

165 tains sensory neurons that transmit pain and itch information up to the brain.

166 ch transmits afferent pain, temperature, and itch information up to the brain.

167 Itch, initiated by the activation of sensory neurons, is

168 sory input, yet which spinal neurons process itch input and how itch signals are encoded within the s

169 difelikefalin had a significant reduction in itch intensity and improved itch-related quality of life

170 to 10, with higher scores indicating greater itch intensity).

171 n the weekly mean score on the 24-hour Worst Itching Intensity Numerical Rating Scale (WI-NRS; scores

172 Mechanical itch is a desire to scratch due to light mechanical stim

173 Itch is a distinct aversive sensation that elicits a str

174 Itch is a highly prevalent and multidimensional symptom.

175 Itch is a unique sensation that helps organisms scratch

176 Recurrent and intractable chronic itch is a worldwide problem, but mechanisms, especially

177 of astrocytes in the pathogenesis of chronic itch is also emerging.

178 Itch is an aversive sensation that evokes a desire to sc

179 Itch is induced chemically in the peripheral nervous sys

180 ever, the role of TRPC4 in acute and chronic itch is still largely unknown.

181 ed as mast cell receptors, but their role in itch is unclear.

182 Chronic itch, defined as itch lasting longer than 6 weeks, is a highly prevalent

183 ereas their chemogenetic excitation elicited itch-like behaviors and facilitated responses to several

184 ropic receptors elicits inflammatory pain or itch, making it an attractive target for novel analgesic

185 ing the hypothesis that other novel effector itch mechanisms derived from mast cells are important.

186 Classically, our understanding of itch mechanisms has centered around the canonical IgE-ma

187 induce spontaneous colitis upon transfer to Itch(+/+) mice but aggravated chemically induced colitis

188 Microbiota of Itch(-/-) mice failed to induce spontaneous colitis upon

189 t Bacteroides vulgatus, which is expanded in Itch(-/-) mice, was sufficient to induce colon inflammat

190 s sufficient to induce colon inflammation in Itch(-/-) mice.

191 expansion of colitogenic Bacteroides sp. in Itch(-/-) mice.

192 ubstantially reduced colonic inflammation in Itch(-/-) mice.

193 ing analysis of mouse spinal cord in chronic itch models induced by squaric acid dibutylester and imi

194 hrough which a distinct E3 ubiquitin ligase, ITCH, modulates DDR machinery in triple-negative breast

195 queductal gray (PAG) neuronal populations in itch modulation in mice.

196 ded cough (n=115, 16%), rash (n=66, 9%), and itching (n=37, 5%).

197 The E3 ubiquitin ligase, ITCH, negatively regulates the tumour suppressor protein

198 Given the superficial localization of itch neuron terminals, cells that dwell close to the ski

199 ly reduces mechanical but not acute chemical itch nor noxious touch information.

200 lation of spinal Grp neurons does not affect itch nor pain transmission, demonstrating that spinal Gr

201 Consistent with these findings, impaired ITCH nuclear translocation and H1.2 polyubiquitination s

202 Rapid reductions in the itch numerical rating scale score occurred within 36 hou

203 nduce unpleasant itch sensations (mechanical itch or alloknesis).

204 injury or during infection, leading to pain, itch, or analgesia.

205 ht breast associated with redness, pain, and itching over the past month (Fig 1).

206 ht breast associated with redness, pain, and itching over the past month.

207 andard deviation = 18.0) in patients without itch (P < 0.001) and 74.9 (standard deviation = 15.7) in

208 andard deviation = 15.6) in controls without itch (P < 0.001).

209 (P < 0.0001) and approached significance for itch (P = 0.052).

210 herapies aimed at blocking the histaminergic itch pathway have been largely ineffective, suggesting t

211 suggesting the existence of nonhistaminergic itch pathways.

212 For chronic itch patients, the affective component of itch affects b

213 that leads to stress and anxiety in chronic itch patients.

214 ous itch are intractable symptoms in chronic itch patients.

215 Much of itch perception is still a mystery, but we present in th

216 Outcome measures were itch (presence, chronicity, and intensity), the Hospital

217 l neural circuits modulate acute and chronic itch processing.

218 pruritus (VAS) and improved the validated 5D-Itch questionnaire (P = .002 vs placebo).

219 ch-responsive amygdala neurons in modulating itch-related affect and behavior.SIGNIFICANCE STATEMENT

220 y restricted ablation of GRP neurons reduced itch-related behaviors to different pruritogens, whereas

221 orrelations with each other as well as other itch-related measures and nonsignificant correlations wi

222 f itch-sensing neurons that express multiple itch-related molecules including MrgprA3, MrgprC11, hist

223 ant reduction in itch intensity and improved itch-related quality of life as compared with those who

224 cant improvement from baseline to week 12 in itch-related quality of life as measured by the 5-D itch

225 utcomes included the change from baseline in itch-related quality-of-life measures, the percentage of

226 sponses of sensory neurons and expression of itch-related TRP channels suggest no change in sensory t

227 The contribution of these neurons to spinal itch relay is still only incompletely understood, and th

228 However, the mechanisms causing itch remain poorly understood.

229 Chronic itch remains a highly prevalent disorder with limited tr

230 Squaric acid dibutylester-induced itch requires both nonhistaminergic and histaminergic pa

231 , threshold tracking and histamine flare and itch response and neuropathological examination in some

232 -31) in skin wound tissue during the peak of itch responses.

233 Il31(-/-) mice lacked wound-induced itch responses.

234 These results highlight the importance of itch-responsive amygdala neurons in modulating itch-rela

235 lated quality of life as measured by the 5-D itch scale and the Skindex-10 scale.

236 Itch scores >=4 and VSS scores >7 were considered severe

237 ood samples for genotyping and self-reported itch scores within 1 year of injury.

238 Nemolizumab improved EASI, IGA, and/or NRS-itch scores, with the 30-mg dose being most effective.

239 ing of circuit mechanisms of the unstoppable itch-scratch cycles and shed important insights into chr

240 ecognized gaps in understanding about sleep, itch, scratching, atopic dermatitis, and psoriasis.

241 er understand the relationships among sleep, itching, scratching, and chronic itch conditions and the

242 lation with cowhage induced a more intensive itch sensation compared with stimulation with other subs

243 Itch sensation to histamine injection was lost in most s

244 nor has any such pathway been identified for itch sensation.

245 y discovered circuits also contribute to the itch sensation.

246 h is critical for the maintenance of chronic itch sensation.

247 nown that algogens and cooling could inhibit itch sensation; however, the underlying molecular and ne

248 nd light tactile touch may induce unpleasant itch sensations (mechanical itch or alloknesis).

249 Touch and itch sensations are crucial for evoking defensive and em

250 ons have been identified as one of the major itch-sensing neuronal populations.

251 the unique morphological characteristics of itch-sensing neurons and provide intriguing insights int

252 s revealed the unique molecular signature of itch-sensing neurons and the distinct transcriptional pr

253 nic mouse line, we labeled a small subset of itch-sensing neurons that express multiple itch-related

254 ne phosphatase histochemistry, we found that itch-sensing skin arbors exhibit free endings with exten

255 However, a complete analysis of itch-sensing terminal arborization is missing.

256 itability of Ucn3(+) neurons lead to chronic itch sensitization.

257 n vivo using nanoparticles, and silencing of ITCH sensitizes the tumour cells to irradiation treatmen

258 ls (cDC2s) recruited to wounds and increased itch sensory neuron sensitivity.

259 pathways integrate with recently identified itch-sensory circuits in the nervous system to inform a

260 , and tryptase) and the pattern of activated itch-sensory neurons.

261 ence (MD) -5; 95%CI -7.75 to -2.25), and the itch severity score (ISS)7 (MD -2.15; 95% CI -3.2 to -1.

262 Patients with skin involvement and itch showed the highest levels of ILC2s, which was indep

263 at phosphorylated ERK is a unique marker for itch signal transmission in the spinal cord and an attra

264 Recently, we have revealed itch signaling in DRG neurons by which TRPC4 mediates it

265 related to keratinocyte differentiation and itch signaling.

266 ed scratching while Na(V)1.9 was involved in itch signalling towards 5-HT, C48/80 and SLIGRL.

267 proposed general role of Na(V)1.7 and 1.9 in itch signalling, scrutiny of time courses suggested Na(V

268 ependent diversity in Na(V) channel-mediated itch signalling.

269 ch spinal neurons process itch input and how itch signals are encoded within the spinal cord is not f

270 a xenograft mouse model showed around 15-20% ITCH silencing 48 hours after transfection.

271 Transfection of these cell lines with ITCH siRNA could effectively silence the ITCH expression

272 Finally, in vivo delivery of the ITCH siRNA using nanoparticles to the neuroblastoma xeno

273 ly the neural mechanisms, underlying chronic itch still remain unclear.

274 bpopulation of amygdala neurons responded to itch stimuli such as histamine.

275 ciated with (1) breast pain, (2) bother from itching, stinging/burning, swelling, or hurting of the t

276 Classical itch studies have focused on immunoglobulin E (IgE)-medi

277 In four different mouse models of chronic itch, sustained ERK phosphorylation was detected mainly

278 e Patient-Oriented Scoring Atopic Dermatitis-itch, the Patient-Oriented Scoring Atopic Dermatitis-sle

279 les and shed important insights into chronic itch therapy.

280 y modalities: gentle touch, mechanical pain, itch, thermosensation, and proprioception.

281 ogically, proinflammatory cytokines activate ITCH to maintain BRAF activity and to promote proliferat

282 aling in DRG neurons by which TRPC4 mediates itch to serotonergic antidepressants and demonstrated th

283 erical rating scale (scores range from 0 [no itch] to 10 [worst itch imaginable]).

284 development of itch and the acute-to-chronic itch transition remain unknown.

285 ults significantly increase our knowledge of itch transmission and uncover potential targets for comb

286 iguing insights into the basic mechanisms of itch transmission.

287 are thus positioned at the center of spinal itch transmission.

288 that spinal Grp neurons are dispensable for itch transmission.

289 in coupled receptors play important roles in itch transmission.

290 ch, and GRP sensory neurons are dedicated to itch transmission.

291 Gastrin-releasing peptide (GRP) is a spinal itch transmitter expressed by a small population of dors

292 a ligand of the CXCR3 receptor that promotes itch via activation of sensory neurons, and we find that

293 and qPCR methods, we firstly identified that ITCH was expressed on p53-mutant neuroblastoma cell line

294 e found that expression of a nuclear form of ITCH was significantly increased in human TNBC cell line

295 tiated FITCH trial (Fibrates for cholestatic ITCH) was to assess effects of bezafibrate on pruritus i

296 our understanding of the peripheral basis of itch, we know very little regarding how central neural c

297 Pain, swelling, erythema, and itching were the most commonly reported local symptoms a

298 an inflammatory skin disease associated with itch, which is a troublesome symptom with a few therapeu

299 y, we found that deficiency of the E3 ligase Itch, which leads to spontaneous colitis and rectal prol

300 rons results in attenuated non-histaminergic itch, without impairing histamine-induced itch.