ライフサイエンスコーパス: allergic airway inflammation

1 ite (HDM)-induced allergic sensitization and allergic airway inflammation.

2 human lung and in patients with experimental allergic airway inflammation.

3 y has been implicated in the pathogenesis of allergic airway inflammation.

4 offspring were analyzed in a murine model of allergic airway inflammation.

5 model of Th2-mediated ovalbumin/alum-induced allergic airway inflammation.

6 lammatory effects in a model of DEP-enhanced allergic airway inflammation.

7 ng pollen- and cat dander-induced innate and allergic airway inflammation.

8 o DEP-enhanced house dust mite (HDM)-induced allergic airway inflammation.

9 t PVs might have an underappreciated role in allergic airway inflammation.

10 of pulmonary stem/progenitor cells (PSCs) in allergic airway inflammation.

11 estigated the effect of MD-2s on HDM-induced allergic airway inflammation.

12 ntratracheally (i.t.) administered to induce allergic airway inflammation.

13 R and airway inflammation in an OVA model of allergic airway inflammation.

14 ytokines via STAT6 during the development of allergic airway inflammation.

15 ploring the novel therapeutic approaches for allergic airway inflammation.

16 f ragweed pollen in a physiological model of allergic airway inflammation.

17 ed total IgE and showed adjuvant activity in allergic airway inflammation.

18 lenged BALB/c mice; a commonly used model of allergic airway inflammation.

19 culture assays, and in vivo murine models of allergic airway inflammation.

20 a critical factor in ragweed-pollen-induced allergic airway inflammation.

21 g, but not classic signaling, might suppress allergic airway inflammation.

22 ory cytokine production in a murine model of allergic airway inflammation.

23 tical cytokine involved in the initiation of allergic airway inflammation.

24 ammation using a murine model of OVA-induced allergic airway inflammation.

25 been associated with inflammation including allergic airway inflammation.

26 y the reciprocal roles of Bcl6 and Blimp1 in allergic airway inflammation.

27 s have been implicated in the development of allergic airway inflammation.

28 ne phase, are protected against the onset of allergic airway inflammation.

29 ate IL-33 production and induce TH2-mediated allergic airway inflammation.

30 ted adaptive immune responses in HDM-induced allergic airway inflammation.

31 he development of acute T(H)2-cell-dependent allergic airway inflammation.

32 S3 gene expression significantly ameliorated allergic airway inflammation.

33 contribution of miR-155 in a mouse model of allergic airway inflammation.

34 Abx-treated mice was sufficient to increase allergic airway inflammation.

35 ys is a characteristic feature of asthma and allergic airway inflammation.

36 larizing the Th2 response in mouse models of allergic airway inflammation.

37 ion of Th2 cytokine production in a model of allergic airway inflammation.

38 13 during type-2 innate immune responses and allergic airway inflammation.

39 as evaluated in a mouse model of HDM-induced allergic airway inflammation.

40 gate whether LAPCs have a pathogenic role in allergic airway inflammation.

41 t did not completely reverse the features of allergic airway inflammation.

42 ipitation assays, and house dust mite-driven allergic airway inflammation.

43 ts protective capacities in murine models of allergic airway inflammation.

44 ifferentiation and activation of aaMs during allergic airway inflammation.

45 ponses in a preclinical mouse model of acute allergic airway inflammation.

46 dent suppression of Tregs in vivo to promote allergic airway inflammation.

47 responses, causing house dust mite-mediated allergic airway inflammation.

48 protein level was found to be upregulated in allergic airway inflammation.

49 helminth infection and are also involved in allergic airway inflammation.

50 n, and suppress development of TH2 cells and allergic airway inflammation.

51 ary DC function and the development of acute allergic airway inflammation.

52 d pulmonary recruitment in a murine model of allergic airway inflammation.

53 arget for novel strategies to interfere with allergic airway inflammation.

54 y inflammation in a humanized mouse model of allergic airway inflammation.

55 oles for both histamine 1 and 4 receptors in allergic airway inflammation.

56 s of Tr1 cells in a house dust mite model of allergic airway inflammation.

57 enesis may contribute to the pathogenesis of allergic airway inflammation.

58 nd in the lung alveoli during papain-induced allergic airway inflammation.

59 lls is critical to their ability to moderate allergic airway inflammation.

60 ll responses, dendritic cell maturation, and allergic airway inflammation.

61 tory pathway that inhibits DC activation and allergic airway inflammation.

62 ective responses in parasitic infections and allergic airway inflammation.

63 erapeutic effect of allergen-specific CTL in allergic airway inflammation.

64 eosinophil and neutrophil recruitment during allergic airway inflammation.

65 egulatory T cell independent in the model of allergic airway inflammation.

66 ells can trigger long-term susceptibility to allergic airway inflammation.

67 ells, including Tfr cells, in the context of allergic airway inflammation.

68 p in the Alternaria alternata mouse model of allergic airway inflammation.

69 o mice significantly reduced the severity of allergic airway inflammation.

70 mation and remodeling using a mouse model of allergic airway inflammation.

71 ells after primary sensitization exacerbates allergic airway inflammation.

72 also tested GR/Cav1 crosstalk in a model of allergic airway inflammation.

73 d mice with SCFAs to examine their effect on allergic airway inflammation.

74 e in the pathogenesis of experimental asthma/allergic airway inflammation.

75 tes eosinophil trafficking in the setting of allergic airway inflammation.

76 ostasis but abolished ILC2 activation during allergic airway inflammation.

77 cumulation of eosinophils in the lung during allergic airway inflammation.

78 9 differentiation and in the pathogenesis of allergic airway inflammation.

79 e-derived BDNF mediates these effects during allergic airway inflammation.

80 and TC may occur as an early event promoting allergic airway inflammation.

81 lymphocytes and on the development of acute allergic airway inflammation.

82 icated as central immune modulator promoting allergic airway inflammation.

83 mice, resulting in an impaired DEP-enhanced allergic airway inflammation.

84 o determine the role of endothelial miR-1 in allergic airway inflammation.

85 gulation in a mouse model of house dust mite allergic airway inflammation.

86 erve to limit ILC2 activation and subsequent allergic airway inflammation.

87 the lung and lymph nodes in murine model of allergic airway inflammation.

88 flammation/remodeling in long term models of allergic airway inflammation.

89 IL-33 signaling are regulated by miR-155 in allergic airway inflammation.

90 ffect of Cavbeta antisense and gabapentin in allergic airway inflammation.

91 ng maturation and migration of DC subsets in allergic airway inflammation.

92 ILC2s and TH2 cells attenuates DEP-enhanced allergic airway inflammation.

93 it remains controversial how Notch promotes allergic airway inflammation.

94 xpansion using experimental murine models of allergic airway inflammation.

95 responses in a murine model of DEP-enhanced allergic airway inflammation.

96 e of TPL-2 in house dust mite (HDM)-mediated allergic airway inflammation.

97 methylating agent alleviated exacerbation of allergic airway inflammation.

98 n TH2 functions and their capacity to reduce allergic airway inflammation.

99 matory cytokine IL-10 in local regulation of allergic airways inflammation.

100 gen-specific CTL have a protective effect on allergic airway inflammation, a function thought to be m

101 in and metalloproteinase-8 (Adam8) regulates allergic airway inflammation (AAI) and airway hyperrespo

102 the pathogenesis of murine models of asthma/allergic airway inflammation (AAI) by promoting expressi

103 We developed a murine model of PIT in allergic airway inflammation (AAI) driven by adoptively

104 is critical for house dust mite (HDM)-driven allergic airway inflammation (AAI) in vivo.

105 However, its function in the pathogenesis of allergic airway inflammation (AAI) is not completely elu

106 ophages (MDM) stimulated with HDM and during allergic airway inflammation (AAI) or nematode infection

107 ls was dispensable for successful therapy of allergic airway inflammation (AAI) with dexamethasone.

108 e infected with RSV virus after clearance of allergic airway inflammation (AAI).

109 ely or negatively regulate susceptibility to allergic airway inflammation (AAI).

110 ls and ILC2 on the susceptibility of mice to allergic airway inflammation (AAI).

111 ne (5-HT) is involved in the pathogenesis of allergic airway inflammation (AAI).

112 dendritic cells (DC), to the development of allergic airway inflammation (AAI).

113 Eosinophilia is a hallmark of allergic airway inflammation (AAI).

114 e in the pathogenesis of experimental asthma/allergic airway inflammation (AAI).

115 lungs from mice with ovalbumin (OVA)-induced allergic airway inflammation (AAI).

116 Additionally, in a model of allergic airway inflammation, administration of SAA to t

117 The pathology of ovalbumin-induced acute allergic airway inflammation after adoptive transfer of

118 itization significantly inhibited subsequent allergic airway inflammation after HDM challenge, includ

119 Syk inhibition reduced allergic airway inflammation, airway hyperresponsiveness

120 In allergic airway inflammation, although a chemokine recep

121 there was no effect of ROCK insufficiency on allergic airways inflammation, although both ROCK1 and R

122 We sought to investigate the role of pDCs in allergic airway inflammation and acute asthma exacerbati

123 Allergic airway inflammation and AHR were examined in a

124 13-expressing cell type for the induction of allergic airway inflammation and airway hyperreactivity.

125 cells that mediate IL-9-dependent effects in allergic airway inflammation and anti-tumor immunity.

126 t have investigated the role of platelets in allergic airway inflammation and asthma.

127 n lymphocyte homing, as well as in models of allergic airway inflammation and asthma.

128 en tested in vivo, a chemerin SMAL decreased allergic airway inflammation and attenuated neuropathic

129 s sufficient to mitigate major parameters of allergic airway inflammation and colitis in mice.

130 ncreased inflammation of Map3k8(-/-) mice in allergic airway inflammation and colitis results from re

131 ient for Tet1 in a well-established model of allergic airway inflammation and demonstrated that loss

132 of gammadeltaT cell blockade on established allergic airway inflammation and development of remodell

133 1 bacteria using the ovalbumin (OVA)-induced allergic airway inflammation and dinitrochlorobenzene (D

134 ey mechanism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma eff

135 Treated mice did not have allergic airway inflammation and had no bronchial hyperr

136 dation of beta-catenin and, thus, attenuated allergic airway inflammation and hyperresponsiveness.

137 ecreased lung TH2 responses, and ameliorated allergic airway inflammation and hyperresponsiveness.

138 gs, which was associated with alleviation of allergic airway inflammation and improvement of lung fun

139 py was investigated in mice with established allergic airway inflammation and in a model in which we

140 populations in the respiratory tract impact allergic airway inflammation and lung epithelial repair.

141 ed to play a role in the processes linked to allergic airway inflammation and lung function.

142 tion, we developed a combined model in which allergic airway inflammation and lung IL-4 and IL-13 exp

143 gous post-AIT sera significantly reduced the allergic airway inflammation and matched their IgE-block

144 EP2 axis is an important endogenous brake on allergic airway inflammation and primarily targets T cel

145 els of disease (crystal-induced peritonitis, allergic airway inflammation and psoriasis), we found th

146 xt of OVA-specific immunotherapy reduced the allergic airway inflammation and responsiveness upon OVA

147 40 levels and CHIT1 activity are enhanced in allergic airway inflammation and thus may contribute to

148 and Wnt pathways during early- or late-onset allergic airway inflammation and to address regulatory m

149 unctionality; however, their contribution to allergic airways inflammation and asthma is poorly under

150 nhibition on AHR in a chronic mouse model of allergic airways inflammation and pollutant exposure.

151 ent on two mouse models of allergic disease, allergic airway inflammation, and contact hypersensitivi

152 l and bacterial infection, predisposition to allergic airway inflammation, and development of immune

153 -specific Blimp-1-deficient mice, a model of allergic airway inflammation, and T-cell adoptive transf

154 usion, we show that AEC CARMA3 helps mediate allergic airway inflammation, and that CARMA3 is a criti

155 mite (HDM) resulted in enhanced HDM-mediated allergic airway inflammation, and, importantly, marked a

156 ST2(+) Treg cells in the context of allergic airway inflammation are Blimp1 dependent, expre

157 , intranasal administration of IL-37 ablated allergic airway inflammation as well as cytokine product

158 tant DEP+HDM exposure significantly enhanced allergic airway inflammation, as characterized by increa

159 of LAPCs isolated from mice with established allergic airway inflammation augments the development of

160 in the progression of many diseases such as allergic airway inflammation, autoimmune diseases, and i

161 During allergic airway inflammation, Bcl6 and Blimp1 play dual

162 IL9 promotes T regulatory cell function and allergic airway inflammation, but it has not been extens

163 us studies suggested that ATP is involved in allergic airway inflammation by acting on type 2 puriner

164 Suppression of allergic airway inflammation by allergen-specific CTL wa

165 data suggest that Tet1 inhibits HDM-induced allergic airway inflammation by direct regulation of the

166 ic cells, is critical to induction of asthma/allergic airway inflammation by driving type 2 inflammat

167 hat miR-155 contributes to the regulation of allergic airway inflammation by modulating T(H)2 respons

168 ulation of pathways involved in promotion of allergic airway inflammation by PM.

169 suggest that SP-A aids in the resolution of allergic airway inflammation by promoting eosinophil cle

170 s participates in the regulation of limiting allergic airway inflammation by regulating extracellular

171 duced by antibiotic (Abx) treatment promotes allergic airway inflammation by shifting macrophage pola

172 Allergic airway inflammation can be prevented by stimula

173 We report that in allergic airway inflammation, CCR2 mediated the recruitm

174 Allergic airway inflammation contributes to the airway r

175 As hypothesized, we found that allergic airway inflammation decreased the number of K.

176 We hypothesized that preexisting allergic airway inflammation decreases lung IL-17A expre

177 In mice with allergic airway inflammation, dsRNA challenges caused a

178 CCR7, is required on Treg cells to suppress allergic airway inflammation during the effector phase.

179 CCR4, is required on Treg cells to suppress allergic airway inflammation during the sensitization ph

180 s representing three different phenotypes of allergic airway inflammation-eosinophilic, mixed, and ne

181 These findings show that HDM-induced allergic airway inflammation facilitates neosensitizatio

182 In marked contrast, ovalbumin-induced allergic airway inflammation failed to promote lung GC s

183 t inhibition of lung edema in a rat model of allergic airway inflammation following dry powder inhala

184 we report that, during cockroach Ag-induced allergic airway inflammation, Foxp3(+) Tregs are rapidly

185 tion with S. pneumoniae, Spp1(+/+) mice with allergic airway inflammation had a significantly lower b

186 s, but the role of CD39 and CD39(+) Tregs in allergic airway inflammation has not been elaborated.

187 However, the role of Nur77 in allergic airway inflammation has not been studied so far

188 However, its role in allergic airway inflammation has not yet been elucidated

189 However, the function of Hsp70 in allergic airway inflammation has remained largely unknow

190 In this study, we used mouse models of allergic airway inflammation (house dust mice and Altern

191 rophylactic or therapeutic Syk inhibition on allergic airway inflammation, hyperresponsiveness, and a

192 f its protective immunomodulatory effects on allergic airway inflammation, hyperresponsiveness, and a

193 T sera with IgE-blocking activity ameliorate allergic airway inflammation in a human/mouse chimeric m

194 aimed to investigate the effects of IL-37 on allergic airway inflammation in a mouse model of experim

195 during concurrent pneumococcal infection and allergic airway inflammation in a murine model.

196 e (COX) inhibition by indomethacin augmented allergic airway inflammation in a STAT6-independent mann

197 ted, can lead to sustained susceptibility to allergic airway inflammation in adulthood.

198 linked with pediatric asthma development and allergic airway inflammation in animal models.

199 inflammatory immune response associated with allergic airway inflammation in asthma involves T helper

200 the adaptive immune response associated with allergic airway inflammation in asthma.

201 which EOS may participate in pathogenesis of allergic airway inflammation in asthma.

202 ected WT progeny from allergy, it aggravated allergic airway inflammation in B cell-deficient offspri

203 Lastly, ST2 is required for the exacerbated allergic airway inflammation in Bcl6(fl/fl) Foxp3-Cre mi

204 e dust mite (HDM) extract was used to induce allergic airway inflammation in both wild-type (Spp1(+/+

205 tivates an AhR-Jag1-Notch cascade to promote allergic airway inflammation in concert with proasthmati

206 n the trafficking of monocyte-derived DCs in allergic airway inflammation in cooperation with CCR2.

207 illustrated by the reduction in severity of allergic airway inflammation in Fpr2-KO mice, due to imp

208 s a key mediator governing susceptibility to allergic airway inflammation in infant mice.

209 ression of TH2-related genes in TH cells and allergic airway inflammation in Itk(-/-) mice.

210 vention of Notch signaling by SAHM1 inhibits allergic airway inflammation in mice and is therefore an

211 ated TH cytokine levels, IgE production, and allergic airway inflammation in mice in a Jag1- and Notc

212 sitization and challenge models to establish allergic airway inflammation in mice, followed by the an

213 in the sensitization and effector phases of allergic airway inflammation in mice.

214 Thp5 enhances Th2 responses and exacerbates allergic airway inflammation in mice.

215 ignificantly reduced, resulting in mitigated allergic airway inflammation in response to Der p 1 and

216 nce, males exhibit reduced susceptibility to allergic airway inflammation in response to environmenta

217 CD11b(+)Ly-6C(+) dendritic cells and type 2 allergic airway inflammation in response to house dust m

218 maternal BBP exposure increases the risk for allergic airway inflammation in the offspring by modulat

219 Wogonin administration attenuated allergic airway inflammation in vivo with reductions in

220 a tryptase inhibitor reduced IL-33-dependent allergic airway inflammation in vivo.

221 We used a murine model of allergic airway inflammation in which mice were sensitiz

222 We analyzed the features of allergic airway inflammation in wild-type and NTN(-/-) m

223 D138(+)IL-10(+) cells dramatically decreased allergic airway inflammation in wild-type and Sema4c(-/-

224 the ability of adoptive transfer to restore allergic airways inflammation in ROCK2-insufficient mice

225 erbate but instead inhibited key features of allergic airway inflammation including lung airway and p

226 Allergic airway inflammation, including asthma, is usual

227 In vivo, in a mouse model of allergic airway inflammation, increased airway eosinophi

228 These novel observations suggest that allergic airway inflammation increases FAO in inflammato

229 g compounds may be beneficial in alleviating allergic airway inflammation induced by fungal allergens

230 bacterial lipopolysaccharide, bleomycin, and allergic airway inflammation induced by house dust mites

231 stigated this mechanism in a murine model of allergic airway inflammation induced by OVA (ovalbumin)

232 activated in asthma; however, their role in allergic airway inflammation is not fully understood.

233 For many patients with asthma, allergic airway inflammation is primarily a Th2-weighted

234 Inhibiting allergic airway inflammation is the goal of therapy in p

235 Allergic airway inflammation is triggered by allergen ex

236 osinophils respond to Th2 signals to control allergic airway inflammation is unclear.

237 , specifically miR-155, in the regulation of allergic airway inflammation is unexplored.

238 hway that can limit induction of innate-type allergic airway inflammation mediated by NH cells.

239 Whether allergic airway inflammation mediates the association be

240 In a model of allergic airway inflammation, mice with Etv5-deficient T

241 In a model of ovalbumin-induced acute allergic airway inflammation, mice with induced deletion

242 ole of miR-155 in the regulation of ILC2s in allergic airway inflammation, miR-155 deficient (miR-155

243 Parallel in vivo experiments using an allergic airway inflammation model demonstrated that thi

244 ed basophil activities and recruitment in an allergic airway inflammation model.

245 mation, AHR and airway remodeling in chronic allergic airway inflammation models.

246 in confers robust protective effects against allergic airway inflammation not only in first- but also

247 Allergic airway inflammation of Zc3h12a(-/-) mice was ex

248 A seminal finding was the dependence of allergic airway inflammation on eosinophil-induced recru

249 fore or after initiation of OVA/alum-induced allergic airway inflammation or peanut-induced food alle

250 s house dust mite or ovalbumin in a model of allergic airway inflammation or the TH17-inducing bacter

251 To induce allergic airway inflammation, OVA-pulsed DCs from IL-6-d

252 2 by gene silencing ameliorates experimental allergic airway inflammation, probably via interruption

253 Mice with house dust mite (HDM)-induced allergic airway inflammation received a single intratrac

254 Allergic airway inflammation reduced gut microbial diver

255 f Foxp3(+) regulatory T cells (Tregs) during allergic airway inflammation remains incomplete.

256 elevant to allergic airway inflammation, the Allergic Airway Inflammation Repository.

257 Thus, allergic airway inflammation represents an antifungal de

258 hilia and lung expression of Th17 cytokines, allergic airway inflammation significantly decreased the

259 IL-1R did not affect any of the features of allergic airway inflammation, such as bronchial eosinoph

260 induces eosinophil apoptosis and attenuates allergic airway inflammation, suggesting that it has the

261 al levels in an established model of chronic allergic airways inflammation, suggesting that Syk inhib

262 ar influenza virus infection and exacerbates allergic airway inflammation susceptibility, indicating

263 Furthermore, in an in vivo recall model of allergic airway inflammation that is dependent on memory

264 insights related to mechanisms of asthma and allergic airways inflammation that could eventually lead

265 e of mRNA microarray experiments relevant to allergic airway inflammation, the Allergic Airway Inflam

266 zed settings such as house dust mite-induced allergic airway inflammation, the lack of IRF4 expressio

267 e plays a crucial role in the development of allergic airway inflammation, the therapeutic potential

268 ating the lung transcriptome associated with allergic airway inflammation; therefore, CAR4 has potent

269 role for Hsp70 in hematopoietic cells during allergic airway inflammation; this illustrates the poten

270 or agonist treatment also limited HDM-driven allergic airway inflammation through an action on alveol

271 te that HFD-induced obesity might exacerbate allergic airway inflammation through mechanisms involvin

272 natal mouse model of ovalbumin (OVA)-induced allergic airway inflammation to understand the long-term

273 generating Th2 responses, are susceptible to allergic airway inflammation, type-II autoimmune disease

274 established and studied in a murine model of allergic airway inflammation using lung histology, pulmo

275 pG/CFP downregulated house dust mite-induced allergic airway inflammation via distinct pathways that

276 gnaling pathway licenses the Th2 response in allergic airway inflammation via promoting lymph node eg

277 Ovalbumin-induced allergic airway inflammation was analyzed in offspring f

278 Allergic airway inflammation was assessed in mouse model

279 Allergic airway inflammation was assessed in vivo in an

280 ed lung K. pneumoniae burden associated with allergic airway inflammation was both neutrophil and CCL

281 d intranasally on 1-11 consecutive days, and allergic airway inflammation was evaluated by bronchoalv

282 Chronic allergic airway inflammation was induced following a hou

283 Allergic airway inflammation was induced in the airways

284 Allergic airway inflammation was induced in WT and FHL2-

285 This wogonin-induced reduction in allergic airway inflammation was prevented by concurrent

286 ity was induced by means of HFD feeding, and allergic airway inflammation was subsequently induced by

287 dy the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly

288 Using a murine model of allergic airway inflammation, we dissected the role of I

289 Using a mouse model of allergic airway inflammation, we found that adoptive tra

290 study, using the mouse model of OVA-induced allergic airway inflammation, we identified that PGI2 re

291 elucidate if these fibers also contribute to allergic airway inflammation, we stimulated lung nocicep

292 vities in a preclinical mouse model of acute allergic airway inflammation when administered at the ti

293 T2(+) conventional T cells, strongly promote allergic airway inflammation when transferred into recip

294 A Th2 immune response is central to allergic airway inflammation, which afflicts millions wo

295 y, asthmatics may be prone to develop severe allergic airway inflammation with a mixed Th2/Th17 immun

296 omitant exposure to DEP plus HDM resulted in allergic airway inflammation with increased eosinophilia

297 luated the in vivo activity of Treg cells in allergic airway inflammation with special focus on CCR4

298 osia artemisiifolia) is a strong elicitor of allergic airway inflammation with worldwide increasing p

299 differentially modulated induction of acute allergic airway inflammation, with PS50G but not PS500G

300 orm for the safe and effective inhibition of allergic airway inflammation without the need for nonspe