ライフサイエンスコーパス: allergic airway disease

1 the effector phase in the ovalbumin-induced allergic airway disease.

2 val Ts E/S in vitro and in a murine model of allergic airway disease.

3 robust TH2 inflammation and exacerbation of allergic airway disease.

4 tinct subsets with unique roles in promoting allergic airway disease.

5 espiratory syncytial virus (RSV)-exacerbated allergic airway disease.

6 cal for amplifying viral exacerbation during allergic airway disease.

7 of BPEx had no effect on the development of allergic airway disease.

8 enesis and inflammation in a murine model of allergic airway disease.

9 vation of macrophages and is correlated with allergic airway disease.

10 lungs of asthmatic patients and in mice with allergic airway disease.

11 ion of this pathway in mice with established allergic airway disease.

12 ereas mice treated with R848 did not develop allergic airway disease.

13 acute ovalbumin- and house dust mite-induced allergic airway disease.

14 Ab response and modifies the development of allergic airway disease.

15 xpression associated with the development of allergic airway disease.

16 fine the role of AAMs in the pathogenesis of allergic airway disease.

17 house dust mite (HDM) mouse model of asthma/allergic airway disease.

18 ed in ovalbumin- and house dust mite-induced allergic airway disease.

19 required for the suppression of established allergic airway disease.

20 sential for preventing airway obstruction in allergic airway disease.

21 tic cell cultures and in an in vivo model of allergic airway disease.

22 hlight the importance of the mTOR pathway in allergic airway disease.

23 eactivity (AHR), and ovalbumin (OVA)-induced allergic airway disease.

24 increased apoptosis in 2 distinct models of allergic airway disease.

25 seful tool to combat the rising incidence of allergic airway disease.

26 scription may enhance the risk of developing allergic airway disease.

27 ation in two separate models of Th2-mediated allergic airway disease.

28 s the inflammatory responses associated with allergic airway disease.

29 cule ICOS regulates Th2 effector function in allergic airway disease.

30 s at sites remote from the lung in models of allergic airway disease.

31 ivation and inflammation in a mouse model of allergic airway disease.

32 utritional modifications in a mouse model of allergic airway disease.

33 re not protected from developing OVA-induced allergic airway disease.

34 uman subjects and mice, ultimately promoting allergic airway disease.

35 -induced inflammation in mice as a model for allergic airway disease.

36 ty and prevent the development of Th2-driven allergic airway disease.

37 sitization and the subsequent development of allergic airway disease.

38 hils via CCR3 have a central role in chronic allergic airway disease.

39 ms by which Gimap5 deficiency predisposes to allergic airway disease.

40 te neutrophils in the pathogenesis of fungal allergic airway disease.

41 nes have not previously been associated with allergic airway disease.

42 l microbiota in promoting the development of allergic airway disease.

43 e the inflammatory processes associated with allergic airway disease.

44 ines in the establishment and maintenance of allergic airway disease.

45 e chemokine receptors CCR3, CCR4 and CCR8 in allergic airway disease.

46 s critical for Th2-mediated responses during allergic airway disease.

47 nesis of inflammation in this mouse model of allergic airway disease.

48 when administrated to mice with established allergic airway disease.

49 ss the biological role of CCR8 in a model of allergic airway disease.

50 to determine its contribution in a model of allergic airway disease.

51 t of airway inflammation in a mouse model of allergic airway disease.

52 elease of mediators involved in inflammatory allergic airway disease.

53 fecting Th2 differentiation in this model of allergic airway disease.

54 ntioxidants and NOX inhibitors in mitigating allergic airway disease.

55 production in a murine model of OVA-induced allergic airway disease.

56 k ICOS/B7RP-1 interactions in a Th2 model of allergic airway disease.

57 effector Th cells into naive mice to induce allergic airway disease.

58 sponses that arise from A. fumigatus-induced allergic airway disease.

59 in part to the absence of chronic models of allergic airway disease.

60 mucin-stimulating activity of lung fluids in allergic airway disease.

61 ragweed are important in the development of allergic airway disease.

62 th PC receptors in the lung protects against allergic airway disease.

63 ived CD4 T cells in a mouse model of chronic allergic airway disease.

64 the other CCR7 ligand, CCL19, has a role in allergic airway disease.

65 e directions for epigenetic investigation in allergic airway disease.

66 ibition of SOCE is a potential treatment for allergic airway disease.

67 ovalbumin-induced severe, steroid-resistant allergic airway disease.

68 siveness and restored steroid sensitivity to allergic airway disease.

69 lay an essential role in neutrophil-dominant allergic airway disease.

70 iotic metabolite for potential prevention of allergic airway disease.

71 the onset and chronic phase of experimental allergic airway disease.

72 ced AR and in an HDM-induced murine model of allergic airway disease.

73 exacerbating effects of antifungal drugs on allergic airway disease.

74 tis, and also exacerbated the development of allergic airway disease.

75 nt to that of uricase inhibited NO2-promoted allergic airway disease.

76 a in human subjects and with mouse models of allergic airway disease.

77 signalling in AEC regulated key features of allergic airway disease.

78 ytes, and in mice enhance the development of allergic airway disease.

79 ollen and potentially increase occurrence of allergic airway disease.

80 cytokines IL-4 and IL-13 and is activated in allergic airway disease.

81 isin that potentially contribute to initiate allergic airway disease.

82 ring the pathophysiology of asthma and other allergic airway diseases.

83 ian populations are increasingly affected by allergic airway diseases.

84 alternative candidate to adult MSCs to treat allergic airway diseases.

85 ght be a therapeutic target in patients with allergic airway diseases.

86 een perceived as a terminal effector cell in allergic airway diseases.

87 hus may contribute to the pathophysiology of allergic airway diseases.

88 ) is the only disease-modifying treatment in allergic airway diseases.

89 g of alarmin biology with a primary focus on allergic airway diseases.

90 em can be considered a therapeutic target in allergic airway diseases.

91 33 in regulating airway immune responses and allergic airway diseases.

92 key cytokine involved in type 2 immunity and allergic airway diseases.

93 P is a promising potential approach to treat allergic airway diseases.

94 way inflammation in patients with asthma and allergic airway diseases.

95 promotes the development and aggravation of allergic airway diseases.

96 the developing immune system and initiating allergic airway diseases.

97 g therapeutic approaches in the treatment of allergic airway diseases.

98 rested mice that previously developed murine allergic airway diseases.

99 Th2-dependent responses in murine models of allergic airways disease.

100 DAMTS-12 functions in experimental models of allergic airways disease.

101 of AAIT for the management and prevention of allergic airways disease.

102 and molecules that suppress IL-17-dependent allergic airways disease.

103 strain matched controls in the OVA model of allergic airways disease.

104 ant but heterogeneous effects on features of allergic airways disease.

105 onhuman primates with experimentally induced allergic airways disease.

106 in both human asthma and in murine models of allergic airways disease.

107 Rho kinases (ROCKs) contribute to allergic airways disease.

108 al role in the initiation and propagation of allergic airways disease.

109 r HDM-induced glycolysis and pathogenesis of allergic airways disease.

110 of susceptibility to fungal allergen-induced allergic airways disease.

111 n HDM-induced glycolysis and pathogenesis of allergic airways disease.

112 ant for maintenance of immune homeostasis in allergic airways disease.

113 he regulation of RSV-induced exacerbation of allergic airways disease.

114 elium of asthmatic patients and in mice with allergic airways disease.

115 metaplasia in a mast cell-dependent model of allergic airways disease.

116 ole in the etiology of eczema and associated allergic airways diseases.

117 irway tolerance compromised in patients with allergic airway diseases?

118 wing weaning, susceptibility and severity of allergic airway disease (a murine model of human asthma)

119 cells is necessary and sufficient to elicit allergic airway disease, a mouse model with many feature

120 a biphasic ovalbumin (OVA)-induced model of allergic airway disease (AAD) and its subsequent resolut

121 Animal models of allergic airway disease (AAD) and virus-induced AAD exac

122 (C57BL/6J), ovalbumin (OVA)-induced model of allergic airway disease (AAD) at early (3-day OVA-aeroso

123 Asthma is an allergic airway disease (AAD) caused by aberrant immune

124 followed throughout time the development of allergic airway disease (AAD) in both uninfected mice an

125 play an important role in the progression of allergic airway disease (AAD) or asthma.

126 B-cell responses and have been implicated in allergic airway disease (AAD).

127 ected to acute OVA aerosol exposures develop allergic airway disease (AAD).

128 ammatory responses during the development of allergic airway disease (AAD).

129 ute to lung inflammation in a mouse model of allergic airway disease (AAD).

130 rum and lung tissue of mice with and without allergic airway disease (AAD).

131 en early life gut fungal dysbiosis and later allergic airway disease (AAD).

132 icant role in the pathogenesis of asthma and allergic airway disease (AAD).

133 ust particles (DEP) predisposed offspring to allergic airway disease (AAD, murine counterpart of huma

134 Asthma is an allergic airways disease (AAD) caused by dysregulated im

135 aride and pneumolysoid (T+P), which suppress allergic airways disease (AAD) in mouse models of asthma

136 HDM-induced allergic airways disease (AAD) in neonatal ST2(-/-) mice

137 a steroid-sensitive, house dust mite-induced allergic airways disease (AAD) model and a steroid-insen

138 ss (AHR) and inflammation in mouse models of allergic airways disease (AAD), associated with inductio

139 ciency on the development of murine neonatal allergic airways disease (AAD).

140 llergen-driven and rhinovirus 1B-exacerbated allergic airways disease (AAD).

141 This leads to the development of allergic airway disease after allergen rechallenge, wher

142 pha(-/lox) mice in chronic ovalbumin-induced allergic airway disease, airway hyperreactivity, T(H)2 r

143 of asthma, but the role of Th17 response in allergic airway disease and aging is not well understood

144 gnaling are unnecessary for the induction of allergic airway disease and AHR.

145 airway proteinase activity to initiate both allergic airway disease and antifungal immunity.

146 ate and adaptive immune responses in chronic allergic airway disease and identify T2M cells as a new

147 Herein we show that pendrin plays a role in allergic airway disease and in regulation of ASL thickne

148 aternal 25(OH)D concentration on outcomes of allergic airway disease and lung function at 20 to 25 ye

149 n D (25[OH]D) concentrations and outcomes of allergic airway disease and lung function in offspring w

150 Additionally, at age 20 years, outcomes of allergic airway disease and lung function were assessed

151 -NO2 is efficacious in preclinical models of allergic airway disease and may have potential for treat

152 ), produced by B cells, is a key molecule in allergic airway disease and plays an important role in T

153 exacerbated lung inflammation in a model of allergic airway disease and promoted higher Th2 response

154 were chronically exposed to HDM to establish allergic airway disease and then treated with the EGFR i

155 ils infiltrate airway walls in patients with allergic airway diseases and in animal models of these i

156 pollution (TRAP) exposure is associated with allergic airway diseases and reduced lung function in ch

157 mined in peripheral blood from subjects with allergic airways disease and controls as well as with in

158 ave been linked mechanistically in models of allergic airways disease and have been associated with a

159 a exacerbations, we combined mouse models of allergic airways disease and human rhinovirus infection.

160 s (ODNs), which mimic bacterial DNA, inhibit allergic airways disease and promote responses in the sp

161 e were found to be protected from developing allergic airways disease and showed a marked decrease in

162 ons, and is implicated in obesity, diabetes, allergic airway disease, and altered immune function.

163 nstrated therapeutic effects, on established allergic airway disease, and prevented the development o

164 AAIT can alter the progression of childhood allergic airways disease; and (4) propose a study design

165 e suggest that the severity and character of allergic airway disease are age dependent, with a bias t

166 s by which respiratory infections facilitate allergic airway disease are incompletely understood.

167 Allergen sensitization and allergic airway disease are likely to come about through

168 Allergic airway diseases are immune disorders associated

169 acid (OA-NO2) reduced the severity of murine allergic airway disease, as assessed by various patholog

170 ded significant relief from establishment of allergic airways disease, as evident from attenuated Th2

171 wever, both groups of mice exhibited similar allergic airway disease at day 12 after the conidia chal

172 ypically protects against the development of allergic airway disease but may be overcome to induce al

173 thought to contribute to the pathogenesis of allergic airway disease by virtue of their decreased NO

174 However, whether COX inhibition can promote allergic airway diseases by inhibiting immune tolerance

175 plays a crucial role in the pathogenesis of allergic airways disease by increasing IL-1beta-induced

176 Allergic airway disease caused by house dust mites or ov

177 viral epitopes in virus inoculated mice with allergic airway disease compared to mice treated with vi

178 ression of CRTh2 was higher in subjects with allergic airways disease compared to controls (P < 0.05)

179 Airway macrophages from mice with allergic airways disease demonstrate a change in activat

180 Dermatophagoides farinae-dependent model of allergic airway disease, dextran sodium sulfate-induced

181 sed IL-4Ralpha, those induced in vivo during allergic airway disease did not, possibly rendering them

182 ologic inhibition, may modulate Th2-mediated allergic airway disease differently.

183 In mice with established allergic airway disease, EGFR inhibition reduced levels

184 IL-10 signaling in virus-infected mice with allergic airway disease enhanced pulmonary CD4(+) T cell

185 volvement of innate lymphoid cells (ILCs) in allergic airway disease exacerbation caused by high-fat

186 HFD feeding exacerbated allergic airway disease features, including humoral resp

187 Murine models of allergic airways disease for asthma research have recent

188 Here we show that in a murine model of allergic airway disease, genetic deletion of the C3a rec

189 nvironmental factors and immune responses in allergic airway diseases, identification of new allergen

190 ttenuated inflammatory responses redeveloped allergic airway disease if the OVA aerosols were interru

191 During acute allergic airway disease, IL-4 deficiency did not prevent

192 In contrast, TNF was dispensable for allergic airway disease in a protease-mediated model of

193 sufficient for the development of long-term allergic airway disease in mice and implies that deregul

194 associated with significant exacerbation of allergic airway disease in mice, including an increase i

195 ng in a striking decrease in the severity of allergic airway disease in mice.

196 role that T reg cells play in the control of allergic airway disease in mice.

197 lung ameliorates established fungal-induced allergic airway disease in mice.

198 ell hyperplasia characterizes fungal-induced allergic airway disease in mice.

199 s characteristic Th2 and Th17 cell-dependent allergic airway disease in mice.

200 etary intake of methyl donors on the risk of allergic airway disease in offspring in mice and show th

201 through their mother's milk with RSV induced allergic airway disease in response to OVA sensitization

202 and risk factors for the high prevalence of allergic airway disease in the tropical urban environmen

203 n attention for the increasing prevalence of allergic airway diseases in Europe.

204 with allergens in starting and exacerbating allergic airway diseases in part by production of reacti

205 the pathogenesis of house dust mite-induced allergic airways disease in C57BL/6NJ mice.

206 To determine the role of DARC in allergic airways disease in mice, and the association be

207 d e-cigarettes, with or without nicotine, on allergic airways disease in mice.

208 ) to reverse the increased susceptibility to allergic airways disease in neonatal mice in a model of

209 to each allergen was assessed in a model of allergic airways disease in which treated mice were prot

210 tivated exhibited characteristic features of allergic airway disease, including airway eosinophilia a

211 r management of eosinophilic inflammation in allergic airway disease, including asthma.

212 tudies in human subjects and mouse models of allergic airway disease indicate a central role of IL-33

213 etect a role for NLRP3 in the development of allergic airway disease induced by either acute or chron

214 In mice we utilized a model of allergic airways disease induced by house dust mite to d

215 Clinical allergic airway disease is associated with persistent ai

216 Allergic airway disease is characterized by a robust lym

217 A. fumigatus-induced allergic airway disease is characterized by persistent a

218 the development and maintenance of Th2-type allergic airway disease is controversial.

219 ntaining (NLR) family, to the development of allergic airway disease is currently controversial.

220 However, its role in asthma and allergic airway disease is largely unknown.

221 It is well known that allergic airways disease is characterized by inflammatio

222 hyperresponsiveness in RV-infected mice with allergic airways disease is directed in part by eotaxin-

223 We review studies of murine allergic airway disease (MAAD) and human asthma that eva

224 In certain models of allergic airway disease, mast cells facilitate the devel

225 results suggest that the presence of AAMs in allergic airway disease may be only an association, as a

226 ed the function of CD137 engagement using an allergic airway disease model in which the mice were sen

227 Augmented IFN-gamma responses in the HDM allergic airway disease model were accompanied by increa

228 Applying an ovalbumin-induced allergic airway disease model, we found a dramatic reduc

229 n of tolerogenic dendritic cells (DCs) in an allergic airways disease model.

230 In all of the allergic airway disease models, the NLRP3 inflammasome-a

231 Of interest especially for allergic airway disease, mucosal germs might not just el

232 sion is well established, yet the effects of allergic airway disease on the host response to intra-pu

233 ell subsets in an ovalbumin-induced model of allergic airway disease (OVA-AAD).

234 have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged m

235 sitized with cockroach allergen (CRAg), then allergic airway disease parameters were assessed after C

236 enhanced a variety of parameters relevant to allergic airways disease, possibly by altering NO homeos

237 but the environmental factors that instigate allergic airway disease remain poorly understood.

238 in Ag-driven exacerbation of chronic murine allergic airway diseases remain elusive.

239 gger both type 2 and type 17 inflammation in allergic airway disease, remain unclear.

240 In a mast cell model of allergic airways disease, ROCK1 and ROCK2 both contribut

241 albumin-induced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were dev

242 case inhibited the development of OVA-driven allergic airway disease subsequent to OVA challenge, as

243 as been implicated in the pathophysiology of allergic airway disease such as asthma.

244 Features of allergic airway disease such as mucous cell hyperplasia,

245 on (airway mycosis) is an important cause of allergic airway diseases such as asthma, but the mechani

246 e 2 immunity in the airways and induction of allergic airway diseases such as asthma.

247 se of their known pathophysiological role in allergic airway diseases such as asthma.

248 vo blockade of TIGIT suppressed hallmarks of allergic airway disease, such as lung eosinophilia, gobl

249 e type 2 cytokine IL-13 is a key mediator of allergic airway diseases, such as asthma, and is up-regu

250 nd ILC2 levels are elevated in patients with allergic airway diseases suggest that IL-33 plays an imp

251 In contrast, using two models of allergic airway disease, Th17 cells from the lungs of di

252 nctional role of ceramide in mouse models of allergic airway disease that recapitulate the cardinal c

253 with methyl donors enhanced the severity of allergic airway disease that was inherited transgenerati

254 rapeutic effects in mice with fungal-induced allergic airway disease, the highest dose of IL-13-PE te

255 thought to play pivotal roles in asthma and allergic airway diseases, the immunological mechanisms t

256 s positively associated with the etiology of allergic airways disease, the current findings suggest t

257 ary factors can modify the heritable risk of allergic airway disease through epigenetic mechanisms du

258 can interact with allergens in exacerbating allergic airway diseases through generation of reactive

259 IVIg alleviates allergic airways disease through interaction of SA-IgG w

260 urine model of virus-induced exacerbation of allergic airway disease to examine the role of CCR1 on T

261 mite allergen mucosal sensitization model of allergic airway disease to investigate the role of alveo

262 l transfer of protection from development of allergic airway disease to offspring in this model of ma

263 and the role of ORMDL3 in the generation of allergic airways disease to the fungal aeroallergen Alte

264 ed using B7-DC cross-linking Abs, preventing allergic airway disease upon re-exposure to allergen.

265 uced glycolytic reprogramming contributes to allergic airway disease using a murine house dust mite m

266 essed the role of STAT6 in Th2/Th17-mediated allergic airway disease using STAT6(-/-) mice.

267 can exacerbate or trigger the development of allergic airway diseases via multiple mechanisms dependi

268 t1), the impact of Wnt on the development of allergic airway disease was analyzed.

269 The suppression in allergic airway disease was associated with a marked exp

270 In CCR5-/- mice at day 12, the allergic airway disease was associated with airway hyper

271 An exacerbation model of allergic airway disease was established whereby mice wer

272 ith allergen exposure, or the development of allergic airway disease was evaluated in TLR4 or TRIF kn

273 Allergic airway disease was examined after ovalbumin sen

274 Allergic airway disease was induced in mice by repeated

275 Acute or chronic allergic airway disease was induced in mice using ovalbu

276 Allergic airway disease was induced in wild-type, IL-10

277 with A. fumigatus conidia, and the resulting allergic airway disease was monitored for up to 37 days.

278 echanisms, but whether they might ameliorate allergic airway disease was previously untested.

279 An ovalbumin-induced mouse model of allergic airway disease was used.

280 Allergic airways disease was assessed 24 hours and 7 day

281 nsitized and challenged (OVA) mouse model of allergic airways disease was utilized.

282 (Runx3), a gene known to negatively regulate allergic airway disease, was found to be excessively met

283 hydrogen peroxide in the pathophysiology of allergic airway disease, we comparatively evaluated mice

284 Using a murine model of neutrophil-dominant allergic airway disease, we demonstrate that BET inhibit

285 urine model of house dust mite (HDM)-induced allergic airway disease, we demonstrated that anxa1 prot

286 ive cell transfer studies in mouse models of allergic airway disease, we examined the effects of Act-

287 To investigate the role of IP-10 in allergic airway disease, we examined the expression of I

288 By using a mouse model of allergic airway disease, we have defined in this study t

289 sing a robust murine model of antigen-driven allergic airways disease, we have demonstrated that IVIG

290 llergic sensitizations and family history of allergic airway disease were higher in the high symptom

291 Furthermore, features of allergic airway disease were not induced in allergen-cha

292 rway fibroblasts and mouse models of chronic allergic airway disease were used to evaluate leptin's e

293 , rhesus monkeys with experimentally induced allergic airways disease were treated seven times with i

294 ensitization can be the predominant cause of allergic airway diseases, whereas in other environments,

295 valbumin (OVA) and cockroach (CRA) models of allergic airway disease, which are based predominantly o

296 HDM translates into increased prevalence of allergic airway diseases, which now impact a large propo

297 a mouse model of RSV-induced exacerbation of allergic airways disease, which mimics hallmark clinical

298 uts together our current knowledge on IgE in allergic airway diseases with a special focus on the ide

299 ILC2s to drive the exacerbation of a murine allergic airway diseases with an eosinophilic phenotype.

300 provides a novel therapeutic option to abate allergic airway disease without altering life-saving aut