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

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

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

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

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

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

6 been associated with inflammation including allergic airway inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

19 13 during type-2 innate immune responses and allergic airway inflammation.

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

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

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

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

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

25 ifferentiation and activation of aaMs during allergic airway inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 ective responses in parasitic infections and allergic airway inflammation.

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

45 eosinophil and neutrophil recruitment during allergic airway inflammation.

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

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

48 nses, we used a murine model of self-limited allergic airway inflammation.

49 ne responses that regulate susceptibility to allergic airway inflammation.

50 as investigated in a murine model of chronic allergic airway inflammation.

51 arkedly reduced severity in OVA/alum-induced allergic airway inflammation.

52 panediol (FTY720) can alleviate experimental allergic airway inflammation.

53 itro effector cell proliferation and in vivo allergic airway inflammation.

54 IL-17RB pathway regulates IL-9 expression in allergic airway inflammation.

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

56 nas gingivalis exerts a regulatory effect on allergic airway inflammation.

57 In addition, Arhgef5 deficiency attenuated allergic airway inflammation.

58 fferentiation for the development of AHR and allergic airway inflammation.

59 n a complex real world allergen in mediating allergic airway inflammation.

60 DCs develop airway neutrophilia rather than allergic airway inflammation.

61 ophils to the lung during the development of allergic airway inflammation.

62 chondrial dysfunction in the exacerbation of allergic airway inflammation.

63 ts is responsible for the severe symptoms in allergic airway inflammation.

64 ivity in the lungs of mice with experimental allergic airway inflammation.

65 identify Delta1 as an important regulator of allergic airway inflammation.

66 imera and rhinovirus-induced exacerbation of allergic airway inflammation.

67 kin (IL)-4, -5, and -13 in ovalbumin-induced allergic airway inflammation.

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

69 xpansion using experimental murine models of allergic airway inflammation.

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

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

72 methylating agent alleviated exacerbation of allergic airway inflammation.

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

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

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

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

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

78 icated as central immune modulator promoting allergic airway inflammation.

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

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

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

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

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

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

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

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

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

88 ploring the novel therapeutic approaches for allergic airway inflammation.

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

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

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

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

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

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

95 ays hyperresponsiveness in a murine model of allergic airways inflammation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

112 Syk inhibition reduced allergic airway inflammation, airway hyperresponsiveness

113 In allergic airway inflammation, although a chemokine recep

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

115 In a mouse model of allergic airways inflammation, an increase in peribronch

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

117 Allergic airway inflammation and AHR were examined in a

118 13-expressing cell type for the induction of allergic airway inflammation and airway hyperreactivity.

119 osinophils are central effector cells during allergic airway inflammation and an important clinical t

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

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

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

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

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

125 1 bacteria using the ovalbumin (OVA)-induced allergic airway inflammation and dinitrochlorobenzene (D

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

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

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

129 min A (250-IU/g) diets to the development of allergic airway inflammation and hyperresponsiveness.

130 oid drug dexamethasone in the mouse model of allergic airway inflammation and identified a viridin-de

131 ritical role for mFPR2 in the progression of allergic airway inflammation and immune responses.

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

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

134 n two independent models of allergen-induced allergic airway inflammation and in IL-4 lung transgenic

135 se 3 ligand (Flt3L) reverses the features of allergic airway inflammation and increases a Th2-suppres

136 y regulator of specific hallmark features of allergic airway inflammation and it could be a potential

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

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

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

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

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

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

143 f a regulatory effect of an oral pathogen on allergic airway inflammation and responsiveness.

144 LP) has important roles in the initiation of allergic airway inflammation and the activation of dendr

145 40 levels and CHIT1 activity are enhanced in allergic airway inflammation and thus may contribute to

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

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

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

149 ed lung-specific IL-13 transgenic mice (with allergic airway inflammation) and control mice.

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

151 s of TH2 cytokines and chemokines related to allergic airway inflammation, and enhanced airway hyper-

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

153 fection in humans, including augmentation of allergic airway inflammation, and will be useful in the

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

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

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

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

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

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

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

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

162 thesized that psychosocial stress aggravates allergic airway inflammation by altering innate immune c

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

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

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

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

167 Allergic airway inflammation can be prevented by stimula

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

169 Allergic airway inflammation contributes to the airway r

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

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

172 In allergic airway inflammation, dendritic cells (DCs) are

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

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

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

176 zation may be capable of suppressing AHR and allergic airway inflammation, even in previously sensiti

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

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

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

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

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

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

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

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

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

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

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

188 letion of CARMA1 prevents the development of allergic airway inflammation in a mouse model of asthma

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

190 ergic responses and COX inhibition increases allergic airway inflammation in a STAT6-independent fash

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

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

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

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

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

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

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

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

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

200 h2 polarization may have utility in altering allergic airway inflammation in human asthmatic patients

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

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

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

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

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

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

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

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

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

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

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

212 duction and optimal T-cell proliferation and allergic airway inflammation in vivo.

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

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

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

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

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

218 Allergic airway inflammation, including asthma, is usual

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

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

221 xamined the role of IL-6 in a mouse model of allergic airway inflammation induced by direct airway ex

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

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

224 In addition, chronic allergic airway inflammation induces a pronounced overex

225 Allergic airway inflammation is a disease in which T hel

226 Allergic airway inflammation is characterized by marked

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

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

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

230 Allergic airway inflammation is triggered by allergen ex

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

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

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

234 Whether allergic airway inflammation mediates the association be

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

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

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

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

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

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

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

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

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

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

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

246 2 by gene silencing ameliorates experimental allergic airway inflammation, probably via interruption

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

248 Allergic airway inflammation reduced gut microbial diver

249 The role of inducible NO synthase (iNOS) in allergic airway inflammation remains elusive.

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

251 e-1-phosphate receptors in the regulation of allergic airway inflammation remains undefined.

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

253 Thus, allergic airway inflammation represents an antifungal de

254 T cells are critical mediators of the allergic airway inflammation seen in asthma.

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

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

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

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

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

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

261 In Th2 immunity and allergic airway inflammation, the ability of a DC to fun

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

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

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

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

266 lial-expressed HS plays an important role in allergic airway inflammation through the regulation of r

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

268 e contribution of IL-6 to the development of allergic airway inflammation triggered by inhaled allerg

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

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

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

272 s but plays a role in promoting Th2-mediated allergic airway inflammation via unique effects on lung

273 Effective Th2 generation and allergic airway inflammation was achieved in CD11c/A(bet

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

275 Allergic airway inflammation was assessed in mouse model

276 We show that allergic airway inflammation was associated with an incr

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

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

279 Chronic allergic airway inflammation was induced following a hou

280 Allergic airway inflammation was induced in the airways

281 Allergic airway inflammation was induced in WT and FHL2-

282 eosinophil and neutrophil recruitment during allergic airway inflammation was investigated.

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

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

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

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

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

288 To clarify the role of STAT6 in allergic airway inflammation, we generated mouse bone ma

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

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

291 2 or T(H)17 response and elicited diminished allergic airway inflammation when adoptively transferred

292 ary, we have identified a miRNA signature in allergic airway inflammation, which includes miR-21 that

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

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

295 Additionally, in allergic airway inflammation with ovalbumin sensitizatio

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

297 body formation especially of IgE isotype and allergic airway inflammation with the generation of regu

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