ライフサイエンスコーパス: allergen challenge

1 l IL-4Ralpha-deficient mice after intranasal allergen challenge.

2 ow cytometry before and 7 and 24 hours after allergen challenge.

3 CCL17, CCL22, and CXCL12) in the lung after allergen challenge.

4 ouse asthma models following a physiological allergen challenge.

5 eceived the alternate treatment and repeated allergen challenge.

6 Biopsy samples were taken before and after allergen challenge.

7 assessed mannitol responsiveness 24 h after allergen challenge.

8 h AD have altered tissue immune responses on allergen challenge.

9 f tissue inflammation following cessation of allergen challenge.

10 in peripheral blood after nasal grass pollen allergen challenge.

11 eness was measured before and 24 hours after allergen challenge.

12 challenges were performed 24 h pre- and post-allergen challenge.

13 by flow cytometry before and 24 hours after allergen challenge.

14 lergen-induced gut inflammation after rectal allergen challenge.

15 ergic reaction after segmental endobronchial allergen challenge.

16 hmatics at baseline and 24 h after segmental allergen challenge.

17 R) and airway eosinophilia in mice following allergen challenge.

18 acted maximally at baseline independently of allergen challenge.

19 splenocyte proliferations, and intragastric allergen challenge.

20 DCs) into the draining lymph nodes following allergen challenge.

21 t as well as immunological effects and nasal allergen challenge.

22 exes of airway inflammation before and after allergen challenge.

23 he killer protease granzyme B in response to allergen challenge.

24 MMP-9 in the allergic asthma condition upon allergen challenge.

25 response, as measured 3 to 7 hours after the allergen challenge.

26 rve of FEV1 measured 2-8 h following inhaled allergen challenge.

27 bronchoalveolar lavage fluids (BALFs) after allergen challenge.

28 duced rhinoconjunctivitis after standardized allergen challenge.

29 es previously shown to be up-regulated after allergen challenge.

30 ell chemokines, and inflammatory cells after allergen challenge.

31 pared to unseparated BAL cells after in vivo allergen challenge.

32 sed on each subject's response to whole lung allergen challenge.

33 asthma at baseline and 48 h after segmental allergen challenge.

34 ant change in Th2 cytokines during the final allergen challenge.

35 disposes to IgE-mediated anaphylaxis on oral allergen challenge.

36 RNA levels also increased in BAL cells after allergen challenge.

37 onal Treg cells in the lungs after segmental allergen challenge.

38 B2 and immunoglobulin E at 24 h after local allergen challenge.

39 rtion or nasal volume proportion after nasal allergen challenge.

40 e low within the airways and increased after allergen challenge.

41 and subjective (symptoms) responses to nasal allergen challenge.

42 sensitized with allergen followed by airway allergen challenge.

43 den CD11b(hi)MHCII(hi) DCs in the lung after allergen challenge.

44 at select intervals before or after aerosol allergen challenge.

45 ammation than did wild-type DC after inhaled allergen challenge.

46 aseline bronchoalveolar lavage and segmental allergen challenge.

47 ples were collected before and 5 weeks after allergen challenge.

48 with allergic asthma is studied by bronchial allergen challenge.

49 er dosing, subjects underwent complete nasal allergen challenge.

50 e protein gp120 after sensitization prior to allergen challenge.

51 ines IFN-gamma and TNF-alpha upon intranasal allergen challenge.

52 stic of the pulmonary microenvironment after allergen challenge.

53 nflammation when administered at the time of allergen challenge.

54 avage (BAL) fluid before and after segmental allergen challenge.

55 mediately after IL4M-supplemented AIT during allergen challenge.

56 ed with macrophages from male mice following allergen challenge.

57 es and neutrophil/lymphocyte ratio after the allergen challenge.

58 tively to allergen-sensitized animals before allergen challenge.

59 tients with mild asthma 48 hours after acute allergen challenge.

60 y and immunologically after an environmental allergen challenge.

61 wed by saline-controlled segmental bronchial allergen challenge.

62 ssed in the esophagus, skin, and lungs after allergen challenge.

63 us healthy controls in response to segmental allergen challenge.

64 l mice from anaphylaxis-mediated death after allergen challenge.

65 s in the lung-draining lymph node (LN) after allergen challenge 1 mo later.

66 IL-5 neutralization before allergen challenge abolished the allergen-induced rise i

67 Treatment with gp120 prior to allergen challenge abrogated airway hyperresponsiveness

68 and IL-33 levels were higher in the lungs of allergen-challenged Adamts12-deficient mice.

69 irway hyperresponsiveness) underwent inhaled allergen challenge after 2-hour exposures to DE, particl

70 ard Th1 and Th17 immunity, and protects from allergen challenge after only 2-4 monthly administration

71 y wall thickness aspect ratio (omega) of the allergen-challenged airway was compared with those of si

72 The allergen-challenged airway was lavaged 24 h later.

73 sampling and sensitive detection techniques, allergen challenge allows the study of several features

74 fective in suppressing the response to nasal allergen challenge, although it was insufficient for inh

75 ld dust results in protection against airway allergen challenge and a distinct gastrointestinal micro

76 vascularity, and stool after oral or rectal allergen challenge and a strong histologic inflammation

77 cumulate in the airway-adjacent region after allergen challenge and are activated by the accumulated

78 in allergic asthma subjects after segmental allergen challenge and are related to increased pro-fibr

79 cs underwent methacholine challenge, inhaled allergen challenge and endobronchial allergen provocatio

80 allergic asthmatic patients after segmental allergen challenge and in esophageal biopsy specimens fr

81 and sputum eosinophils before and after the allergen challenge and in the fraction of exhaled nitric

82 ammation was induced by rectal or intranasal allergen challenge and monitored by mini endoscopy or ai

83 ted in bronchoalveolar cells and fluid after allergen challenge and mRNA levels correlated with prote

84 veolar lavage fluid 48 hours after segmental allergen challenge and strongly correlated with the incr

85 ed impaired lung IL-33 levels in response to allergen challenge and the number of ILC2s was significa

86 d CCL18 levels were elevated after segmental allergen challenge and these levels correlated with thos

87 rols are increased in inflamed airways after allergen challenge and, through G-protein subunit alpha,

88 Inhaled allergen challenges and skin tests were conducted before

89 or of PAR2 signalling, pepducin, i.n. before allergen challenges and then assessed AHR and airway inf

90 s known to accumulate in the lung, following allergen challenge, and contributes via activation of pu

91 measured before and at 7 and 24 hours after allergen challenge, and methacholine airway responsivene

92 line challenge, on Day 3 they had an inhaled allergen challenge, and on Days 4 and 6 they had sputum

93 ts, reduced airway resistance in response to allergen challenge, and reduced IL-13 cytokine levels in

94 tion resulted in RhoA activity in vivo after allergen challenge, and RhoA signaling in platelets thro

95 antly blunted the physiological responses to allergen challenge, and this effect persisted for at lea

96 g sensitization, immediately after AIT under allergen challenge, and two weeks post-treatment.

97 ic asthma underwent methacholine and inhaled allergen challenges, and endobronchial allergen provocat

98 y specimens were collected after intradermal allergen challenges, and late-phase responses were measu

99 ng function and bronchial inflammation after allergen challenge are well known, little has been repor

100 ation in the lungs upon in vivo transfer and allergen challenge, as Notch-deficient Th2 cells were re

101 Using allergen-challenge assays, we found that SIT treatment d

102 placebo, provides improved nasal response to allergen challenge at 3-year follow-up.

103 m placebo in improving the nasal response to allergen challenge at 3-year follow-up.

104 SLPR mAb for 6 weeks, and their responses to allergen challenge at baseline, week 2, and week 6 were

105 A(min)) after bolus (ragweed) complete nasal allergen challenge at screening were studied by using a

106 lergic skin inflammation induced by repeated allergen challenge, at least in part, via effects on CD8

107 pants with mild allergic asthma by segmental allergen challenge before and 1 month after a single int

108 ion of 1NMPP1 in TrkBKI mice during the 4-wk allergen challenge blunted airway hyperresponsiveness (A

109 endritic cells (DCs) around the airway after allergen challenge but very limited access of these airw

110 mber of group 2 innate lymphoid cells during allergen challenge but was not required for establishmen

111 specificity reduced all airway responses to allergen challenge by 82-96% (p </= 0.001) and fully nor

112 lergy reduced anaphylactic responses to oral allergen challenge by 84% to 90%, as well as diarrhea, m

113 those in cell counts obtained 24 h after the allergen challenge by a bronchoalveolar lavage of the re

114 for TSLP in amplifying Th2 responses during allergen challenge by direct action on CD4 T cells; howe

115 on their surface and immediately respond to allergen challenge by releasing inflammatory mediators.

116 rs) and 6 hours and 24 hours after segmental allergen challenge by using either normal- or low-dose a

117 Allergen challenge caused an early change (0-2 h) in min

118 IL-4/IL-13 levels were markedly increased in allergen-challenged Cd300f(-/-) mice, a finding that is

119 d a putative intermediary TF, namely ETS1 in allergen-challenged CD4(+) cells from allergic patients.

120 ETS1 increased significantly in allergen-challenged CD4(+) cells from patients compared

121 IRF4 and its target genes were examined in allergen-challenged CD4(+) cells from patients with IAR,

122 IRF4 increased in allergen-challenged CD4(+) cells from patients with IAR,

123 Increased expression of IRF4 in allergen-challenged CD4(+) cells from patients with inte

124 TSLP responses were not required during oral allergen challenge, CD4(+) T cells were required and tra

125 atients were exposed to both allergens in an allergen challenge chamber (ACC) before and after 9 mont

126 rs per day to house dust mite allergen in an allergen challenge chamber (ACC).

127 nyssinus) powder on 4 consecutive days in an allergen challenge chamber.

128 e dust mite (HDM) allergen in the Fraunhofer allergen challenge chamber.

129 change in eosinophil pH-buffering capacity, allergen-challenged chimeric mice that contained Car4(-/

130 in early and late-phase symptoms after every allergen challenge compared to diluent (both P < .05) wi

131 in in patients with mild atopic asthma after allergen challenge compared with diluent control.

132 ated enhanced IL-33 secretion in response to allergen challenge compared with values seen in nasal ep

133 ggest that elevation of ceramide level after allergen challenge contributes to the apoptosis, reactiv

134 Conversely, allergen challenge decreased airway responsiveness to ma

135 ied mRNA either before or after the onset of allergen challenge, demonstrating its potential as both

136 es, but such effect declined under sustained allergen challenge despite a persistent presence of mese

137 in EOS(A) relative to blood EOS from airway allergen-challenged donors.

138 t altered between EOS(A) and EOS from airway allergen-challenged donors.

139 AHR and airway resistance, was diminished in allergen-challenged doxycycline-exposed compared with no

140 Furthermore, in an allergen-challenged environment, in vivo phosphorylation

141 Additionally, following allergen challenge, EOS(A) express significantly more CI

142 After repeated allergen challenge, eosinophils appeared not essential f

143 enetic changes upon exposure in a controlled allergen challenge facility, and identified baseline epi

144 of ovalbumin (OVA) sensitization and airway allergen challenges followed by assessment of inflammati

145 V1 was measured repeatedly for 7 hours after allergen challenge for early and late asthmatic response

146 an CD33, and desensitized mice to subsequent allergen challenge for several days.

147 samples obtained before and after segmental allergen challenge from patients with mild asthma and in

148 llagen around the lung bronchioles after Ova-allergen challenge further confirmed the protective role

149 In vivo, allergen-challenged Gal-1-deficient mice exhibited incre

150 ly demonstrated that ERp57 is upregulated in allergen-challenged human and murine lung epithelial cel

151 However, in response to allergen challenge, IL-33 is rapidly released into BALFs

152 However, after multiple daily allergen challenges, IL-17 production and AHR decreased,

153 o eosinophils from both untreated and fungal allergen-challenged IL5tg mice, which undergo rapid demi

154 ional blockade of PAR2 in the airways during allergen challenge improves allergen-induced AHR and inf

155 ronchoalveolar lavage fluid, after segmental allergen challenge in allergic asthmatic patients.

156 cantly improved ARC symptoms after rye grass allergen challenge in an EEU with an acceptable safety p

157 Both allergen challenge in individuals with allergic asthma a

158 rated asthma progression induced by viral or allergen challenge in later life.Conclusions: Pneumoviru

159 Novel repetitive nasal allergen challenge in participants with severe persisten

160 Chitosan exposure, prior to rDer p2 allergen challenge in passively sensitized mice, resulte

161 of the inflammatory response after segmental allergen challenge in patients with asthma and may serve

162 ung-derived ILC2s before and after segmental allergen challenge in patients with mild-to-moderate ast

163 oinflammatory cytokine secretion after final allergen challenge in sensitized mice.

164 granulation, and allergic symptoms caused by allergen challenge in sensitized mice.

165 To assess the role of ILC2s during nasal allergen challenge in subjects with allergic rhinitis us

166 bserved in nasal mucosa following intranasal allergen challenge in the GPA group but not in SCIT and

167 d altered transcriptional programs following allergen challenge in vivo.

168 er expression of M2 genes in vitro and after allergen challenge in vivo.

169 use mast cell protease 1 (mMCP-1) induced by allergen challenge in WT mice and expression of mMCP-4,

170 long-lived within the lung after PIT, before allergen challenge, in contrast to CD62L(hi) Th2 cells.

171 Allergen challenge increased airway responsiveness to me

172 Delivery of 5 x 10(5) purified nTreg reduced allergen challenge-induced airway IL-4 (p </= 0.03) and

173 2-specific IgE (P < 0.05), as well as midge allergen-challenge-induced scratch bouts, midge allergen

174 Allergen challenge induces a 127-fold increase in ORMDL3

175 Because allergen challenge induces lung ORMDL3 expression in wil

176 , administration of IL-33trap at the time of allergen challenge inhibits inflammatory responses in a

177 in 1 and 2 secretion in response to repeated allergen challenge is myeloid cell A(2B) R dependent.

178 Standardized allergen challenge is primarily a research tool, and whe

179 Nasal allergen challenge is sensitive in the detection of clin

180 IL-33 increased secretion of serotonin from allergen-challenged isolated airways.

181 Q, sV(A), and Fgas in the allergen-challenged lobe were compared with the right up

182 ymus, spleen, uterus, peritoneal cavity, and allergen-challenged lung.

183 Selection of a particular allergen challenge method should depend on consideration

184 Interestingly, allergen-challenged Mgat5(-/-) mice developed airway neu

185 Allergen-challenged Mgat5-deficient (Mgat5(-/-)) mice ex

186 hat the increases in lung ceramide levels in allergen-challenged mice are not mediated by oxidative s

187 tion in the lungs of allergen-sensitized and allergen-challenged mice compared with WT control animal

188 Eosinophils recruited to the airways of allergen-challenged mice express ORMDL3.

189 Alternatively, allergen-challenged mice received intranasal rhinovirus-

190 ility of CD11b(hi) DCs in the draining LN of allergen-challenged mice to induce proliferation of OVA-

191 ivity, exacerbates airway hyperreactivity in allergen-challenged mice, providing evidence for a prote

192 rker profiles, and recirculation behavior in allergen-challenged mice, which had been pretreated with

193 s of SOCS3 were reduced in asthmatics and in allergen-challenged mice.

194 At the time of allergen challenge, mice received topical intranasal tre

195 roduction, was upregulated in the airways of allergen-challenged miR-155 KO mice compared with WT mic

196 number of ILC2s was significantly reduced in allergen-challenged miR-155(-/-) mice compared with WT m

197 enous injection of IL-33 or pulmonary fungal allergen challenge mobilized ILC2 progenitors to exit th

198 ted a potent selective CCR4 antagonist in an allergen challenge model of canine AD, both clinically a

199 mation (40 mg/kg qd) as well as a guinea pig allergen challenge model of lung inflammation (20 mg/kg

200 We used a human experimental allergen challenge model, with flow cytometric analysis

201 er and inflammation on Feno values using the allergen challenge model.

202 ase in the number of lung T(reg) cells in an allergen challenge model.

203 The direct-instillation nasal allergen challenge (NAC) and the environmental exposure

204 Nasal allergen challenge (NAC) is a human model of allergic rh

205 The nasal allergen challenge (NAC) is a useful tool for the diagno

206 ry mediators in nasal fluids following nasal allergen challenge (NAC), whereas the effects of NAC on

207 t group) were subjected to consecutive nasal allergen challenges (NAC) with seasonal (NAC-S) and pere

208 Nasal allergen challenges (NACs) and allergic biomarker assess

209 tometry, and our results showed that neither allergen challenge nor monoclonal antibody therapy alter

210 -sugars, respectively-were upregulated after allergen challenge, notably in airway epithelial cells,

211 (BAL) during late-phase responses following allergen challenge of allergic subjects.

212 e human airway after bronchoscopic segmental allergen challenge of asthmatic patients.

213 Whole-lung allergen challenge of atopic asthma patients revealed va

214 mucosa increased significantly after in vivo allergen challenge of patients with allergic rhinitis.

215 ent activation and tissue inflammation after allergen challenge of sensitized mice.

216 bility in allergen-induced airway responses, allergen challenge offers an adequate disease model for

217 mg twice daily) or placebo for 7 days, with allergen challenge on day 7.

218 We conducted allergen challenges on days 42 and 84 to evaluate the ef

219 en postnatal days 21 and 35, prior to airway allergen challenges on days 48, 49, and 50.

220 Eleven mild atopic asthmatics completed allergen challenges on two separate occasions.

221 alter the inflammatory response to segmental allergen challenge or clinical measures of asthma sympto

222 Accordingly, pDC depletion after allergen challenge or during rhinovirus infection abroga

223 johnsonii protected them against both airway allergen challenge or infection with respiratory syncyti

224 f the Wnt antagonist Dickkopf-1 (Dkk-1) upon allergen challenge or non-healing parasitic infection.

225 this process was IL-25, which was induced by allergen challenge or rhinovirus infection and condition

226 ion in airway hyperresponsiveness (AHR), OVA allergen-challenged Ormdl3(Delta2-3/Delta2-3)/CC10 mice

227 s, but numbers increased significantly after allergen challenge (P < .05), whereas at the same time,

228 C of IgE-blocking factor correlated to nasal allergen challenge (p = 0.63, P = .0012) and SPT (p = 0.

229 nasal instillation of eotaxin-2/CCL24 before allergen challenge partially restored airway eosinophili

230 Overexpression of Wnt during the allergen challenge phase attenuated the development of a

231 ization but exerted their effect at the lung allergen challenge phase by inhibiting expansion of CD11

232 TNF was also required during the allergen challenge phase for neutrophilic and eosinophil

233 ng the inhibitor during the sensitization or allergen challenge phases in the primary challenge model

234 e abatacept or placebo, followed by a second allergen challenge protocol after 3 months of study drug

235 By use of a novel human repetitive nasal allergen challenge (RAC) model, we evaluated the relatio

236 inhibitor (Compound 20) administered during allergen challenge reduced ILC2 numbers and activation,

237 of ovalbumin-sensitized mice with pLR during allergen challenge reduced the acute asthma phenotype.

238 irway eosinophil and Th2 responses to recall allergen challenge remained approximately 85-95% suppres

239 ctively, and by 46 and 34% at 24 hours after allergen challenge, respectively, versus placebo (all P

240 well as blood DCs after in vivo and in vitro allergen challenge, respectively.

241 atory infiltrates, antibody treatment during allergen challenge resulted in a marked relative increas

242 Allergen challenge resulted in airway inflammation as ev

243 In AR patients, local allergen challenge resulted in increases in pDC and mDC

244 In vitro or in vivo allergen challenge resulted in rapid airway epithelial I

245 ing at sites of inflammation after segmental allergen challenge (SAC).

246 After allergen challenge, several genes promoting type 2 infla

247 In proof-of-efficacy studies thus far, allergen challenge showed a fair positive predicted valu

248 phagocytes sorted after 1 week of continued allergen challenge showed an activated phenotype at leas

249 activated bronchoalveolar Eos obtained after allergen challenge showed elevated survival and Pin1 act

250 BAL was performed in both saline and allergen-challenged sites 20-24 h. after challenge.

251 ors that promotes immune cell recruitment to allergen-challenged skin.

252 Allergen-challenged SP-A(-/-) mice that received SP-A th

253 Allergen challenge stimulated P release into the airways

254 hmatics in separate dose-ranging studies and allergen-challenge studies.

255 After an allergen challenge, subjects with atopy displayed rapid

256 adoptive transfer of AvCystatin-Mreg before allergen challenge suppressed allergen-specific IgE leve

257 , recruitment of eosinophils to the lungs of allergen-challenged Swap-70(-/-) mice, compared with wil

258 The allergen challenge test has been the mainstay of diagnos

259 Nasal and cutaneous allergen challenge tests were performed annually.

260 lenge showed a group of genes upregulated by allergen challenge that strongly overlapped with 11 gene

261 When compared with non-atopics after allergen challenge the difference between the two groups

262 lpropionitrile (DPN, ER-beta agonist) before allergen challenge to determine IL-33 gene expression an

263 s-like skin lesion, followed by intragastric allergen challenge to induce experimental food allergy.

264 ness, and regional K(i) 10 h after segmental allergen challenge to the right middle lobe in 6 asthmat

265 need for clinicians undertaking higher risk allergen challenges to be able to manage cases of severe

266 airway hyperresponsiveness at 24 hours after allergen challenge versus placebo (P < 0.05).

267 hronic inflammatory diseases are directed by allergen challenge via FcepsilonRI as well as the nature

268 Suppression of allergic responses to cat allergen challenge was associated with significant incre

269 Allergen challenge was continued during HOCl hydrogel ap

270 mpact of OIT on anaphylaxis elicited by oral allergen challenge was determined.

271 oint at the end of day 4 when the cumulative allergen challenge was greatest (P = 0.02).

272 Allergen challenge was performed 1 h post-dose on day 21

273 An allergen challenge was performed before and after the 28

274 Nasal allergen challenge was performed before treatment, at 1

275 Bronchoscopically directed segmental allergen challenge was performed on 24 subjects followed

276 Allergen challenge was performed on day 6 (2 h postdose)

277 Allergen challenge was performed on Day 6.

278 Segmental allergen challenge was performed with saline and allerge

279 AHR 24 h after allergen challenge was significantly reduced with FF/VI

280 ensitization and reactions triggered by oral allergen challenge, we found that EPIT induced sustained

281 f LL-37, 1,25(OH)(2)D, and 25(OH)D following allergen challenge were correlated with each other (P <

282 d <700 IU/mL) with a significant response to allergen challenge were treated with omalizumab accordin

283 Nasal allergen challenges were performed in non-atopic and pol

284 bronchoscopies and inhaled methacholine and allergen challenges were repeated.

285 ies from patients with allergic asthma after allergen challenge, where it correlates with the count o

286 ming receptors and infiltrate the skin after allergen challenge, where they produce the type 2 cytoki

287 to the nasal mucosa within hours after local allergen challenge, whereas conventional dendritic cells

288 d airway hyperresponsiveness (AHR) following allergen challenge, whereas mice sensitized using protea

289 x-expanded Treg cells could be recalled upon allergen challenge, which was associated with suppressio

290 inophils from the lungs and spleen of fungal allergen-challenged wild-type mice are capable of prolon

291 As shown here, eosinophils from fungal allergen-challenged wild-type mice maintain a distinct c

292 eosinophil cultures from the lungs of fungal allergen-challenged wild-type mice.

293 A single bronchial allergen challenge with HDM is accompanied by increased

294 Five weeks after bronchial allergen challenge with HDM, the amount of circulating I

295 ust mite (HDM) allergy underwent a bronchial allergen challenge with HDM.

296 In a murine model, allergen challenge with house dust mite leads to rapid T

297 mice led to reduced lung eosinophilia after allergen challenge, with a broadly reprogrammed immunoac

298 , significantly reduces the late response to allergen challenge, with a trend to reduce airway inflam

299 increased AHR and serum IgE levels following allergen challenge without differences in two outcomes o

300 s obtained before and 48h after a whole lung allergen challenge (WLAC).