ライフサイエンスコーパス: allergen challenge

1 ed with macrophages from male mice following allergen challenge.

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

3 lergen-induced gut inflammation after rectal allergen challenge.

4 ergic reaction after segmental endobronchial allergen challenge.

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

6 acted maximally at baseline independently of allergen challenge.

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

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

9 exes of airway inflammation before and after allergen challenge.

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

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

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

13 bronchoalveolar lavage fluids (BALFs) after allergen challenge.

14 duced rhinoconjunctivitis after standardized allergen challenge.

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

16 ell chemokines, and inflammatory cells after allergen challenge.

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

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

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

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

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

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

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

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

25 rtion or nasal volume proportion after nasal allergen challenge.

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

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

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

29 at select intervals before or after aerosol allergen challenge.

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

31 aseline bronchoalveolar lavage and segmental allergen challenge.

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

33 with allergic asthma is studied by bronchial allergen challenge.

34 er dosing, subjects underwent complete nasal allergen challenge.

35 e protein gp120 after sensitization prior to allergen challenge.

36 tively to allergen-sensitized animals before allergen challenge.

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

38 stic of the pulmonary microenvironment after allergen challenge.

39 row-derived dendritic cells (BMDCs) prior to allergen challenge.

40 er T cells (T(H)17 cells) and less AHR after allergen challenge.

41 s a source of IL-4 in the lung after chronic allergen challenge.

42 ant inhibition of the late phase response to allergen challenge.

43 hat were repeatedly exposed to stress before allergen challenge.

44 hmatic airway inflammation following inhaled allergen challenge.

45 des specifically in response to TH2-inducing allergen challenge.

46 and downregulated in the lung in response to allergen challenge.

47 defective airway neutrophilia in response to allergen challenge.

48 responses were monitored 48 h after the last allergen challenge.

49 des specifically in response to TH2-inducing allergen challenge.

50 have a role in the physiological response to allergen challenge.

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

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

53 y and immunologically after an environmental allergen challenge.

54 wed by saline-controlled segmental bronchial allergen challenge.

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

56 us healthy controls in response to segmental allergen challenge.

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

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

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

60 ouse asthma models following a physiological allergen challenge.

61 eceived the alternate treatment and repeated allergen challenge.

62 Biopsy samples were taken before and after allergen challenge.

63 assessed mannitol responsiveness 24 h after allergen challenge.

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

65 f tissue inflammation following cessation of allergen challenge.

66 in peripheral blood after nasal grass pollen allergen challenge.

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

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

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

70 2 cytokine production and Th2-biased AHRs to allergen challenge 1 mo later.

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

72 Treatment with gp120 prior to allergen challenge abrogated airway hyperresponsiveness

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

74 The study goals were 1) to evaluate how allergen challenge affects lung expression of cav1 and t

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

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

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

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

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

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

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

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

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

84 h1 and Th2 cytokine levels in the lung after allergen challenge and found that pulmonary expression o

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

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

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

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

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

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

91 increased significantly 48 h after segmental allergen challenge and were highly correlated with BAL e

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

93 Inhaled allergen challenges and skin tests were conducted before

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

95 eosinophil-dependent manner in the lungs of allergen-challenged and interleukin (IL)-13-overexpressi

96 ge-derived chemokine/CCL22 in the lung after allergen challenge, and blockade of these chemokines inh

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

98 phils by IL-5 or related cytokines following allergen challenge, and further demonstrate the key role

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 Thus, airway allergen challenge differentially affects two distinct s

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

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

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

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

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

143 After repeated allergen challenge, eosinophils appeared not essential f

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

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

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

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 ing pattern, we used endobronchial segmental allergen challenge in human atopic asthmatics to define

158 in vivo was implicated in a study of airway allergen challenge in patients with allergic asthma.

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

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

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

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

163 eosinophilic airway inflammation 48 h after allergen challenge in these mice was associated with inc

164 d altered transcriptional programs following allergen challenge in vivo.

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

166 or chemoattractants produced during repeated allergen challenge in vivo.

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

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

169 Allergen challenge increased airway responsiveness to me

170 We confirmed that the OVA-allergen challenge increased eosinophilia and T-helper t

171 vessel density that was noted within 48 h of allergen challenge, indicating an early switch to an ang

172 Repeated allergen challenge induced biosynthesis of gVPLA2 in air

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

174 2-specific IgE (P < 0.05), as well as midge allergen-challenge-induced scratch bouts, midge allergen

175 Allergen challenge induces a 127-fold increase in ORMDL3

176 and that the transfer of these BMDCs before allergen challenge induces airway hyperresponsiveness (A

177 Because allergen challenge induces lung ORMDL3 expression in wil

178 HC-030031, when administered during airway allergen challenge, inhibited eosinophil infiltration an

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

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

181 Nasal allergen challenge is sensitive in the detection of clin

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

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

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

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

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

187 ivity in the bronchoalveolar lavage fluid in allergen-challenged mice after oral dosing.

188 th fibroblasts derived from lungs of chronic allergen-challenged mice and not from those derived from

189 r in fibroblasts grown from lungs of chronic allergen-challenged mice compared to fibroblasts grown f

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

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

192 Alternatively, allergen-challenged mice received intranasal rhinovirus-

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

194 The interaction of fibroblasts from chronic allergen-challenged mice with eosinophils also increased

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

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

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

198 Allergen-challenged Mmp7(-/-) mice had less airway hyper

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

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

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

202 A chronic allergen challenge model provided evidence that EPC recr

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

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

205 ry in guinea pig LTB(4) and nonhuman primate allergen challenge models.

206 In an acute allergen challenge murine asthma model, EPC mobilization

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

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

209 Nasal allergen challenges (NACs) and allergic biomarker assess

210 rculating leukocytes in lung microvessels of allergen-challenged Ndst1-deficient mice was significant

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

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

213 Allergen-challenged null mice showed increased lung eosi

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

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

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

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

218 n of naive lung CD4(+)CD25(+) T cells before allergen challenge of sensitized mice, similar to the ad

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 Beagles), AD can be reliably reproduced upon allergen challenge, providing a tool with which to study

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

239 Allergen challenge reduced lung cav1 mRNA abundance by 4

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

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

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

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

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

245 Allergen challenge resulted in airway inflammation as ev

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

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

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

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

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

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

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

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

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

255 Allergen challenge stimulated P release into the airways

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

257 After an allergen challenge, subjects with atopy displayed rapid

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

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

260 The allergen challenge test has been the mainstay of diagnos

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

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

263 allergic airway disease were not induced in allergen-challenged TLR2-/- and MyD88-/- mice exposed to

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

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

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

267 Allergen challenge was continued during HOCl hydrogel ap

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

269 Inhaled allergen challenge was done before and after 4 weeks of

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

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

272 An allergen challenge was performed before and after the 28

273 Nasal allergen challenge was performed before treatment, at 1

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

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

276 Allergen challenge was performed on Day 6.

277 Segmental allergen challenge was performed with saline and allerge

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

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

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

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

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

283 bronchoscopies and inhaled methacholine and allergen challenges were repeated.

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

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

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

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

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

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

290 IL-5 levels in the esophagus of EE patients, allergen-challenged wild-type mice, and CD2-IL-5 transge

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

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

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

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

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

296 ckout (KO) mice were subjected to repetitive allergen challenge with OVA up to 12 wk, and bronchoalve

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).