ライフサイエンスコーパス: airway inflammation

1 y occur as an early event promoting allergic airway inflammation.

2 s in a murine model of DEP-enhanced allergic airway inflammation.

3 as significantly greater during eosinophilic airway inflammation.

4 ation and antibody production during chronic airway inflammation.

5 2 in house dust mite (HDM)-mediated allergic airway inflammation.

6 ng agent alleviated exacerbation of allergic airway inflammation.

7 a strategy for modulating exuberant mucosal airway inflammation.

8 mation are poorly predictive of eosinophilic airway inflammation.

9 ctions and their capacity to reduce allergic airway inflammation.

10 e undergoing IL-33-dependent allergen-driven airway inflammation.

11 n implicated in the pathogenesis of allergic airway inflammation.

12 ed levels of FeNO, a marker for eosinophilic airway inflammation.

13 were analyzed in a murine model of allergic airway inflammation.

14 ite having little effect on lung function or airway inflammation.

15 D4 T cells express Foxp3 during neutrophilic airway inflammation.

16 control mice responded with a marked AHR and airway inflammation.

17 truction in the context of chronic asthmatic airway inflammation.

18 tes and on the development of acute allergic airway inflammation.

19 ic obstructive pulmonary disease (COPD)-type airway inflammation.

20 roid treatment, and evidence of eosinophilic airway inflammation.

21 ction, airway hyperresponsiveness (AHR), and airway inflammation.

22 ced MD2-dependent allergic sensitization and airway inflammation.

23 ass and increased fibrosis in the absence of airway inflammation.

24 central immune modulator promoting allergic airway inflammation.

25 n-1/2-deficient mice led to angiogenesis and airway inflammation.

26 rtially reduced neutrophil numbers and total airway inflammation.

27 Th2-mediated ovalbumin/alum-induced allergic airway inflammation.

28 losely related to the degree of eosinophilic airway inflammation.

29 generation of proinflammatory cytokines and airway inflammation.

30 TH17-like cells and protected against severe airway inflammation.

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

32 te whether hemostatic markers correlate with airway inflammation.

33 turn facilitates allergic sensitization and airway inflammation.

34 ctivate endothelial cells, angiogenesis, and airway inflammation.

35 tes to respiratory infections and pathologic airway inflammation.

36 ncer in the absence or presence of COPD-type airway inflammation.

37 - and cat dander-induced innate and allergic airway inflammation.

38 anced house dust mite (HDM)-induced allergic airway inflammation.

39 occurs within hours of challenge and before airway inflammation.

40 ht have an underappreciated role in allergic airway inflammation.

41 c Th2 memory cells and their contribution to airway inflammation.

42 ary stem/progenitor cells (PSCs) in allergic airway inflammation.

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

44 active in patients with active eosinophilic airway inflammation.

45 ns, innate cytokine release and neutrophilic airway inflammation.

46 eally (i.t.) administered to induce allergic airway inflammation.

47 ophilic (>/=53%) and/or eosinophilic (>/=3%) airway inflammation.

48 assive local and systemic anaphylaxis and on airway inflammation.

49 way inflammation in an OVA model of allergic airway inflammation.

50 via STAT6 during the development of allergic airway inflammation.

51 he novel therapeutic approaches for allergic airway inflammation.

52 indirect stimuli correlates positively with airway inflammation.

53 tify Nur77 as a novel therapeutic target for airway inflammation.

54 pollen in a physiological model of allergic airway inflammation.

55 IgE and showed adjuvant activity in allergic airway inflammation.

56 failed to confer protection against AHR and airway inflammation.

57 sulting in an impaired DEP-enhanced allergic airway inflammation.

58 oid-resistant airway hyperresponsiveness and airway inflammation.

59 nt in asthma features related to the AHR and airway inflammation.

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

61 been shown to down-regulate allergen-induced airway inflammation.

62 imit ILC2 activation and subsequent allergic airway inflammation.

63 and lymph nodes in murine model of allergic airway inflammation.

64 obstruction, airway hyperresponsiveness, and airway inflammation.

65 n/remodeling in long term models of allergic airway inflammation.

66 gnaling are regulated by miR-155 in allergic airway inflammation.

67 Cavbeta antisense and gabapentin in allergic airway inflammation.

68 tion and migration of DC subsets in allergic airway inflammation.

69 L-33-induced ILC2 expansion and eosinophilic airway inflammation.

70 s in the setting of HDM-induced eosinophilic airway inflammation.

71 d TH2 cells attenuates DEP-enhanced allergic airway inflammation.

72 using experimental murine models of allergic airway inflammation.

73 n seen as mediators of widespread continuous airway inflammation, a process known as neurogenic infla

74 al for house dust mite (HDM)-driven allergic airway inflammation (AAI) in vivo.

75 spensable for successful therapy of allergic airway inflammation (AAI) with dexamethasone.

76 m mice with ovalbumin (OVA)-induced allergic airway inflammation (AAI).

77 d with RSV virus after clearance of allergic airway inflammation (AAI).

78 gatively regulate susceptibility to allergic airway inflammation (AAI).

79 athology of ovalbumin-induced acute allergic airway inflammation after adoptive transfer of BMDCs was

80 Mice deficient in Sema4C exhibited increased airway inflammation after allergen exposure, with massiv

81 are known to contribute to these changes in airway inflammation after Mycoplasma pulmonis infection

82 Airway inflammation, AHR, resistance, and compliance wer

83 Syk inhibition reduced allergic airway inflammation, airway hyperresponsiveness, and pul

84 e have a phenotype of increased eosinophilic airway inflammation, allergic sensitization, TH2 cytokin

85 e- or double-deficient mice had eosinophilic airway inflammation and a TH2 cell activation phenotype

86 to investigate the role of pDCs in allergic airway inflammation and acute asthma exacerbations.

87 gammaT supplementation reduces eosinophilic airway inflammation and acute neutrophilic response to i

88 prior to Ag challenge effectively prevented airway inflammation and AHR in an Ag-specific manner.

89 data show that Sul-121 effectively inhibits airway inflammation and AHR in experimental COPD models,

90 sing cell type for the induction of allergic airway inflammation and airway hyperreactivity.

91 Using mouse models of O3-induced airway inflammation and airway hyperresponsiveness (AHR)

92 eveloped mixed eosinophilic and neutrophilic airway inflammation and airway hyperresponsiveness (AHR)

93 tenin in mice largely attenuated HDM-induced airway inflammation and airway hyperresponsiveness to me

94 and IgE antibodies, airway hyperreactivity, airway inflammation and airway remodelling.

95 standing that PCFs are involved in long-term airway inflammation and airway resistance after RSV infe

96 Airway inflammation and airway resistance were evaluated

97 Knowledge of the aging effect on airway inflammation and asthma control is limited.

98 ver, to what extent these cells can regulate airway inflammation and asthma remains to be elucidated.

99 educed ovalbumin- or house-dust-mite-induced airway inflammation and bronchial hyperresponsiveness.

100 ent to mitigate major parameters of allergic airway inflammation and colitis in mice.

101 The effect of Neu5Gc was examined in murine airway inflammation and colitis models, and the role of

102 ing from reduced SIgA contributes to chronic airway inflammation and disease progression.

103 ng the role of eNO in epithelial function or airway inflammation and disease.

104 ism by which TAS2R agonists blocked allergic airway inflammation and exerted anti-asthma effects.

105 aused a pronounced inhibition of HDM-induced airway inflammation and goblet cell hyperplasia.

106 ulmonary CD11c(+) cells induces neutrophilic airway inflammation and hyperreactivity.

107 re to pollutants, such as ozone, exacerbates airway inflammation and hyperresponsiveness (AHR).

108 ovirus-induced neutrophilic and eosinophilic airway inflammation and hyperresponsiveness were reduced

109 Asthma is defined by airway inflammation and hyperresponsiveness, and contrib

110 lung TH2 responses, and ameliorated allergic airway inflammation and hyperresponsiveness.

111 Airway inflammation and hypersensitivity as well as dela

112 ge differences in LT and Wnt pathways during airway inflammation and identify a steroid-resistant cas

113 the pathogenesis of allergen-induced type 2 airway inflammation and identify cellular sources of the

114 rt a protective role of Nur77 in OVA-induced airway inflammation and identify Nur77 as a novel therap

115 SplD-induced airway inflammation and IgE production were largely depe

116 was associated with alleviation of allergic airway inflammation and improvement of lung function.

117 vestigated in mice with established allergic airway inflammation and in a model in which we neutraliz

118 uced ILC2 numbers and activation, as well as airway inflammation and IRF4 and NFAT1 expression.

119 Inhaled endotoxin induces airway inflammation and is an established risk factor fo

120 Fevipiprant reduces eosinophilic airway inflammation and is well tolerated in patients wi

121 We sought to compare airway inflammation and its relationship to asthma contr

122 We sought to compare airway inflammation and its relationship to asthma contr

123 spiratory pathogen known to cause a range of airway inflammation and lung and extrapulmonary patholog

124 ry gene expression is related to patterns of airway inflammation and lung function and identify molec

125 y a role in the processes linked to allergic airway inflammation and lung function.

126 COPD is characterized by chronic airway inflammation and lung infections.

127 -AIT sera significantly reduced the allergic airway inflammation and matched their IgE-blocking activ

128 The lung tissues were assessed for airway inflammation and mucus secretion.

129 Asthma is related to airway inflammation and oxidative stress.

130 ings suggest a novel mechanism that promotes airway inflammation and pathologies in response to CS ex

131 ductions in sputum P. aeruginosa density and airway inflammation and produced modest improvements in

132 odel of cockroach extract (CE)-mediated AHR, airway inflammation and remodeling in BALB/c mice.

133 gement occurred independently of features of airway inflammation and remodeling, whereas it was assoc

134 ion to prevent house dust mite (HDM)-induced airway inflammation and remodeling.

135 mplex disease with heterogeneous features of airway inflammation and remodeling.

136 ich might represent a therapeutic target for airway inflammation and remodeling.

137 l presentation and the type and intensity of airway inflammation and remodelling.

138 , CCL2, CCL3, and CCL4, as well as increased airway inflammation and responsiveness.

139 Exhaled nitric oxide (eNO) is a biomarker of airway inflammation and seems to precede respiratory sym

140 fect of oral corticosteroids on FEV1 , Pc20, airway inflammation and serum cytokines was investigated

141 important role in the pathogenesis of type 2 airway inflammation and suggests therapeutic improvement

142 eceptor 7/8 suppresses ILC2-mediated AHR and airway inflammation and that depletion of pDCs reverses

143 Studies comparing airway inflammation and the airway microbiome are sparse

144 The study provides evidence that airway inflammation and the frequency of respiratory sym

145 IL-33 influences the development of chronic airway inflammation and tissue remodeling.

146 athways during early- or late-onset allergic airway inflammation and to address regulatory mechanisms

147 ity; however, their contribution to allergic airways inflammation and asthma is poorly understood.

148 RELM-beta has been implicated in airways inflammation and remodelling in murine models.

149 ng disease activity and help in the study of airway inflammation, and asthma severity.

150 irway hyperresponsiveness, mucus production, airway inflammation, and IL-13-induced gene expression.

151 y in mouse models of autoimmune diabetes and airway inflammation, and increased the proportion of Fox

152 h antibodies reduced mortality, weight loss, airway inflammation, and pulmonary viral load.

153 Bronchial hyperreactivity, airway inflammation, and sensitization were significantl

154 show that AEC CARMA3 helps mediate allergic airway inflammation, and that CARMA3 is a critical signa

155 flammasome in the pathogenesis of dermal and airway inflammation, and they highlight the utility of C

156 During eosinophilic airway inflammation, approximately 30% of lung-infiltrat

157 OS, persistent alloimmune injury and chronic airway inflammation are suggested.

158 ar cytokine signaling molecule that promotes airway inflammation as a damage-associated molecular pat

159 Allergen challenge resulted in airway inflammation as evidenced by increased immune cel

160 allenged with OVA show significantly reduced airway inflammation as evidenced by reduced infiltration

161 ds, fluticasone inhibited rhinovirus-induced airway inflammation as evidenced by suppressed BAL neutr

162 HDM exposure significantly enhanced allergic airway inflammation, as characterized by increased airwa

163 Lung M2 macrophages are regulators of airway inflammation, associated with poor lung function

164 esponsiveness and had histologic evidence of airway inflammation (asthma).

165 and effectively inhibited Th2 responses and airway inflammation both prophylactically and therapeuti

166 ID3 prevented airway hyperresponsiveness and airway inflammation (both neutrophilia and eosinophilia)

167 ith chronic asthma resulted in resolution of airway inflammation but not airway hyperreactivity or re

168 cific molecules that suppress CXCL12-induced airway inflammation by acting on G-protein-coupled recep

169 tivity that contributes to allergenicity and airway inflammation by activating proteinase-activated r

170 cruitment to allergic airways and suppresses airway inflammation by inhibiting cell migration and pro

171 ens play a crucial protective role in type 2 airway inflammation by negatively regulating ILC2 homeos

172 f pathways involved in promotion of allergic airway inflammation by PM.

173 s demonstrate a novel function for IL-17A in airway inflammation by showing for the first time that I

174 Activation of pDCs alleviates AHR and airway inflammation by suppressing ILC2 function and sur

175 Differences in airway inflammation can contribute to diminished asthma

176 Airway inflammation causes mucociliary dysfunction.

177 Mice fed R gnavus developed airway inflammation, characterized by expansion of T-hel

178 3(-/-)) mice exhibited significantly reduced airway inflammation compared to wild-type mice.

179 This finding suggests that eosinophilic airway inflammation contributes to COPD exacerbations.

180 The level of eosinophilic airway inflammation correlates with variations in the mi

181 Whether the pattern of airway inflammation differs between African American and

182 Neutrophilic airway inflammation, disease severity, and steroid resis

183 oss asthmatic patients, whereas neutrophilic airway inflammation does not.

184 fection in asthma induces varying degrees of airway inflammation (e.g. neutrophils), but the underlyi

185 rs may be a noninvasive approach to evaluate airway inflammation, exacerbations, and disease severity

186 ion of lung edema in a rat model of allergic airway inflammation following dry powder inhalation comb

187 Total airway inflammation following HDM did not differ between

188 t that, during cockroach Ag-induced allergic airway inflammation, Foxp3(+) Tregs are rapidly mobilize

189 flammatory diseases, its role in RSV-induced airway inflammation has not been investigated.

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

191 this study, we used mouse models of allergic airway inflammation (house dust mice and Alternaria alte

192 tective immunomodulatory effects on allergic airway inflammation, hyperresponsiveness, and airway rem

193 ic or therapeutic Syk inhibition on allergic airway inflammation, hyperresponsiveness, and airway rem

194 n of Sema3E in the airways and its effect on airway inflammation, hyperresponsiveness, and remodeling

195 ct-induced airway hyperresponsiveness (AHR), airway inflammation, immunoglobulin production, TH2-asso

196 gy to reduce exuberant virus-induced mucosal airway inflammation.IMPORTANCE In the United States, 2.1

197 th IgE-blocking activity ameliorate allergic airway inflammation in a human/mouse chimeric model of r

198 ngeneic human ILC2s through ICOSL to control airway inflammation in a humanized ILC2 mouse model.

199 Because azithromycin attenuated neutrophilic airway inflammation in a murine viral bronchiolitis mode

200 nhibition by indomethacin augmented allergic airway inflammation in a STAT6-independent manner.

201 ve pill (OCP) use, systemic inflammation and airway inflammation in adults with asthma.

202 cin was also effective in inhibiting AHR and airway inflammation in an OVA model of allergic airway i

203 lic and endotoxin (LPS)-induced neutrophilic airway inflammation in animal models and healthy human v

204 HDM) acts on the airway epithelium to induce airway inflammation in asthma.

205 tudy we investigated the association between airway inflammation in asthmatic children and oxidative

206 ve value for the development of eosinophilic airway inflammation in asthmatic children at school age.

207 a useful noninvasive marker of eosinophilic airway inflammation in asthmatics.

208 progeny from allergy, it aggravated allergic airway inflammation in B cell-deficient offspring.

209 ponsiveness (AHR) using a methacholine test, airway inflammation in bronchoalveolar lavage (BAL) and

210 inhaled corticosteroids to impair control of airway inflammation in children with SA.

211 Mechanisms driving persistent airway inflammation in chronic obstructive pulmonary dis

212 ature of asthma, produces spontaneous type 2 airway inflammation in juvenile beta-epithelial Na(+) ch

213 f Notch signaling by SAHM1 inhibits allergic airway inflammation in mice and is therefore an interest

214 ut not of Il4 or Il13, prevented exacerbated airway inflammation in mice expressing Il4ra(R576) (here

215 e model of skin inflammation, and it reduces airway inflammation in mice following acute challenge wi

216 ytokine levels, IgE production, and allergic airway inflammation in mice in a Jag1- and Notch-depende

217 eads to significantly increased TH2-mediated airway inflammation in OVA or HDM murine models of asthm

218 posure to aeroallergens induces eosinophilic airway inflammation in patients with asthma and allergic

219 din D2 receptor 2, might reduce eosinophilic airway inflammation in patients with moderate-to-severe

220 ants from Arg2-deficient mice did not affect airway inflammation in recipient mice, supporting reside

221 s exhibit reduced susceptibility to allergic airway inflammation in response to environmental allerge

222 The extent to which eosinophilic airway inflammation in severe asthma responds to treatme

223 etween the airway microbiome and patterns of airway inflammation in steroid-free patients with asthma

224 BBP exposure increases the risk for allergic airway inflammation in the offspring by modulating the e

225 Wogonin administration attenuated allergic airway inflammation in vivo with reductions in BAL and i

226 quired and sufficient for rhinovirus-induced airway inflammation in vivo.

227 We analyzed the features of allergic airway inflammation in wild-type and NTN(-/-) mice after

228 -10(+) cells dramatically decreased allergic airway inflammation in wild-type and Sema4c(-/-) mice.

229 ity of adoptive transfer to restore allergic airways inflammation in ROCK2-insufficient mice, allergi

230 sone treatment suppresses rhinovirus-induced airways inflammation in vivo but also impairs anti-viral

231 We aimed at investigating whether indices of airway inflammation including fractional exhaled nitric

232 been linked to mechanisms involved in type 2 airway inflammation, including fractional exhaled nitric

233 ese novel observations suggest that allergic airway inflammation increases FAO in inflammatory cells

234 lipopolysaccharide, bleomycin, and allergic airway inflammation induced by house dust mites, pulmona

235 However, the role of TSG-6 in acute airway inflammation is not well understood.

236 Eosinophilic airway inflammation is often present in asthma, and redu

237 Upper airway inflammation is one of the most frequent health c

238 Allergic airway inflammation is triggered by allergen exposure th

239 s respond to Th2 signals to control allergic airway inflammation is unclear.

240 Signatures associated with eosinophilic airway inflammation, mast cells, and group 3 innate lymp

241 can limit induction of innate-type allergic airway inflammation mediated by NH cells.

242 R-155 in the regulation of ILC2s in allergic airway inflammation, miR-155 deficient (miR-155(-/-)) an

243 Airway tolerance and allergen-induced airway inflammation models in mice were used to investig

244 marrow, we used acute allergen exposure and airway inflammation models in mice.

245 ls expressing CCR6, RORgammat, and IL-17A in airway inflammation models in vivo.

246 HR and airway remodeling in chronic allergic airway inflammation models.

247 cluding airway hyperreactivity, eosinophilic airway inflammation, mucus hypersecretion, and Ag-specif

248 ation of LT-HDM-pulsed DCs induced a similar airway inflammation, mucus production, and cytokine prod

249 Asthma is characterized by airway inflammation, mucus secretion, remodeling and hyp

250 Levels of airway inflammation, mucus, fibrosis, and airway smooth

251 The underlying airway inflammation of asthma in this age group likely d

252 Allergic airway inflammation of Zc3h12a(-/-) mice was examined wi

253 used, but did not aggravate the eosinophilic airway inflammation or airway hyper-reactivity.

254 To induce allergic airway inflammation, OVA-pulsed DCs from IL-6-deficient

255 Type 2 airway inflammation plays a central role in the pathogen

256 n a murine sensitization model, resulting in airway inflammation, production of serum IgEs, and induc

257 ms that cause persistent, exaggerated, upper airway inflammation rather than acute resolving illness

258 Allergic airway inflammation reduced gut microbial diversity, whi

259 ) regulatory T cells (Tregs) during allergic airway inflammation remains incomplete.

260 h extract (CRE) in early and later life, and airway inflammation, remodeling, and hyperreactivity ass

261 HDM-induced airway inflammation, remodeling, and Th2/Th17-type cell

262 aling plays a key role in CE-induced AHR and airway inflammation/remodeling in long term models of al

263 dy, SAM-11, after the initial development of airway inflammation significantly inhibited all these pa

264 e production, and allergic sensitization and airway inflammation suggest that PGI2 and its analogue i

265 eosinophil apoptosis and attenuates allergic airway inflammation, suggesting that it has therapeutic

266 severe asthma and is linked to neutrophilic airway inflammation, suggesting that these miRNAs contri

267 M-exposed mothers demonstrate increased AHR, airway inflammation, TH2 cytokine production, and immuno

268 OVA-sensitized mice with SD had more severe airway inflammation than the allergic group with HS.

269 cts were more likely to exhibit eosinophilic airway inflammation than white subjects in the ICS+ grou

270 chronic infection and subsequently in local airway inflammation that is harmful to the lungs.

271 regulates AHR and airway remodeling without airway inflammation through a previously unrecognized pa

272 FD-induced obesity might exacerbate allergic airway inflammation through mechanisms involving ILC2s a

273 TLR2(+) macrophages are sufficient to confer airway inflammation to TLR2(-/-) mice, with the pattern

274 the offspring with a persistently increased airway inflammation up to the F2 generation.

275 on led to TH2 sensitization and eosinophilic airway inflammation upon intranasal HDM challenge.

276 wnregulated house dust mite-induced allergic airway inflammation via distinct pathways that involve n

277 two different models to amplify eosinophilic airway inflammation via induced expression of IL-33 by l

278 , gene expression, mucus hypersecretion, and airway inflammation was assessed by using in vivo models

279 Airway inflammation was assessed by using multicolor flo

280 Allergic airway inflammation was assessed in mouse models of acut

281 Airway inflammation was elicited in participants with mi

282 promised in a platelet-dependent manner, and airway inflammation was essentially abolished, resulting

283 sally on 1-11 consecutive days, and allergic airway inflammation was evaluated by bronchoalveolar lav

284 Chronic allergic airway inflammation was induced following a house dust m

285 Airway inflammation was measured daily as fractional exh

286 Eosinophilic airway inflammation was not significantly different betw

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

288 nduced by means of HFD feeding, and allergic airway inflammation was subsequently induced by means of

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

290 Using a murine model of airway inflammation, we found that allergen-specific CD4

291 sing the mouse model of OVA-induced allergic airway inflammation, we identified that PGI2 receptor (I

292 if these fibers also contribute to allergic airway inflammation, we stimulated lung nociceptors with

293 ay hyperresponsiveness, cytokine levels, and airway inflammation were monitored.

294 resence of IL-33, developed antigen-specific airway inflammation when later challenged in the lung.

295 which CXCL12 affects MUC1 transcription and airway inflammation, which depend on activator of G-prot

296 sthma is characterized by persistent chronic airway inflammation, which leads to mucus hypersecretion

297 erican subjects exhibit greater eosinophilic airway inflammation, which might explain the greater ast

298 xposure to DEP plus HDM resulted in allergic airway inflammation with increased eosinophilia, goblet

299 covery, we note surprisingly extensive lower airway inflammation with persistent viral antigen and ce

300 he safe and effective inhibition of allergic airway inflammation without the need for nonspecific imm