ライフサイエンスコーパス: airway inflammation

1 -induced allergic sensitization and allergic airway inflammation.

2 ated FeNO, suggesting increased eosinophilic airway inflammation.

3 se severity in bronchiectasis during chronic airway inflammation.

4 induced asthma characterized by neutrophilic airway inflammation.

5 luding Tfr cells, in the context of allergic airway inflammation.

6 cells in a house dust mite model of allergic airway inflammation.

7 ay smooth muscle cells decreased AHR but not airway inflammation.

8 Alternaria alternata mouse model of allergic airway inflammation.

9 gnificantly reduced the severity of allergic airway inflammation.

10 peutic agent in conditions with neutrophilic airway inflammation.

11 d remodeling using a mouse model of allergic airway inflammation.

12 Th2 cytokines, goblet cell hyperplasia, and airway inflammation.

13 r primary sensitization exacerbates allergic airway inflammation.

14 -33-induced airway hyperreactivity (AHR) and airway inflammation.

15 ce marker CD38 involved in leukemia and lung airway inflammation.

16 ted GR/Cav1 crosstalk in a model of allergic airway inflammation.

17 th SCFAs to examine their effect on allergic airway inflammation.

18 pathogenesis of experimental asthma/allergic airway inflammation.

19 ophil trafficking in the setting of allergic airway inflammation.

20 ut abolished ILC2 activation during allergic airway inflammation.

21 n of eosinophils in the lung during allergic airway inflammation.

22 a sensitive biomarker of asthma, allergy and airway inflammation.

23 ficantly reduces airway hyper-reactivity and airway inflammation.

24 ntiation and in the pathogenesis of allergic airway inflammation.

25 way fibrosis but did not significantly alter airway inflammation.

26 BDNF mediates these effects during allergic airway inflammation.

27 ng increased IL-33 release and ILC2-mediated airway inflammation.

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

29 losely related to the degree of eosinophilic airway inflammation.

30 failed to confer protection against AHR and airway inflammation.

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

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

33 central immune modulator promoting allergic airway inflammation.

34 ollowing RSV infection and may contribute to airway inflammation.

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

36 oid-resistant airway hyperresponsiveness and airway inflammation.

37 33 signaling in myeloid cells is crucial for airway inflammation.

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

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

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

41 imit ILC2 activation and subsequent allergic airway inflammation.

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

43 obstruction, airway hyperresponsiveness, and airway inflammation.

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

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

46 Cavbeta antisense and gabapentin in allergic airway inflammation.

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

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

49 ne the role of endothelial miR-1 in allergic airway inflammation.

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

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

52 using experimental murine models of allergic airway inflammation.

53 d activation of airway eosinophils, reducing airway inflammation.

54 n is inhibitory in Alternaria-induced innate airway inflammation.

55 33 to increase IL-5 and IL-13 production and airway inflammation.

56 k for novel therapeutic approaches targeting airway inflammation.

57 ich lung macrophages dampen allergen-induced airway inflammation.

58 ns controversial how Notch promotes allergic airway inflammation.

59 g and in patients with experimental allergic airway inflammation.

60 tion in pulmonary ILC2s during IL-33-induced airway inflammation.

61 ric oxide (FeNO) is a marker of eosinophilic airway inflammation.

62 pment of acute T(H)2-cell-dependent allergic airway inflammation.

63 1) or ER-beta (Esr2) increased ILC2-mediated airway inflammation.

64 and particulate matter pollutants to promote airway inflammation.

65 IL-33 release, ILC2 cytokine production, and airway inflammation.

66 okine involved in the initiation of allergic airway inflammation.

67 iprocal roles of Bcl6 and Blimp1 in allergic airway inflammation.

68 xpression significantly ameliorated allergic airway inflammation.

69 airway hyperresponsiveness and eosinophilic airway inflammation.

70 TSLP-mediated T(H)2-cell differentiation and airway inflammation.

71 ted in a mouse model of HDM-induced allergic airway inflammation.

72 pression was characteristic for neutrophilic airway inflammation.

73 a preclinical mouse model of acute allergic airway inflammation.

74 g of phenotyping asthmatic subjects based on airways inflammation.

75 en exposure was associated with eosinophilic airway inflammation 1-2 days after exposure and airway o

76 MDM) stimulated with HDM and during allergic airway inflammation (AAI) or nematode infection in mice.

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

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

79 pathogenesis of experimental asthma/allergic airway inflammation (AAI).

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

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

82 sensitivity, resulting in postnatal skin and airway inflammation after the first allergen encounter.

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

84 The mechanisms by which airway inflammation, airway hyperresponsiveness, and var

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

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

87 pecific IL-22-producing T cells that promote airway inflammation and AHR after antigen challenge, sug

88 acological inhibition of DGK diminished both airway inflammation and AHR in mice and also reduced bro

89 We measured airway inflammation and AHR in wild-type, RAGE(-/-) , TL

90 ut not IL-17A, elicited neutrophil-dominated airway inflammation and AHR in WT mice, suggesting that

91 -17A and TNF-alpha, had neutrophil-dominated airway inflammation and AHR on intranasal OVA challenge.

92 t allergic asthma by simultaneously reducing airway inflammation and AHR though independent mechanism

93 f RGMb completely blocked the development of airway inflammation and AHR, even if treatment occurred

94 b mAb effectively blocked the development of airway inflammation and AHR.

95 2 activity and suppressed Alternaria-induced airway inflammation and AHR.

96 ific serum IgE production, allergic lung and airway inflammation and airway hyper-responsiveness (AHR

97 th anti-RGMb or control mAb and examined for airway inflammation and airway hyperreactivity (AHR), a

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

99 ILC2 responses, airway inflammation and airway hyperresponsiveness were

100 ell activation and restrict allergen-induced airway inflammation and airway hyperresponsiveness.

101 stological features, including subepithelial airway inflammation and alveolar space enlargement, were

102 t mediate IL-9-dependent effects in allergic airway inflammation and anti-tumor immunity.

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

104 its receptor ST2 are contributing factors to airway inflammation and asthma exacerbation.

105 e effects of specific inhibition of NLRP3 on airway inflammation and bacterial clearance in a murine

106 ronic inflammatory disorder characterized by airway inflammation and bronchial hyperresponsiveness.

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

108 inflammation of Map3k8(-/-) mice in allergic airway inflammation and colitis results from reduced ABI

109 the mechanisms by which Rab27 contributes to airway inflammation and cytokine release remain ambiguou

110 Rationale: Lung dysbiosis promotes airway inflammation and decreased local immunity, potent

111 Tet1 in a well-established model of allergic airway inflammation and demonstrated that loss of Tet1 i

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

113 subset of asthmatic patients and might drive airway inflammation and epithelial dysfunction in these

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

115 TEPP46 attenuated IL-1beta-mediated airway inflammation and expression of proinflammatory me

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

117 , in turn resulting in chronic peribronchial airway inflammation and goblet cell metaplasia.

118 Treated mice did not have allergic airway inflammation and had no bronchial hyperreactivity

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

120 ident innate effector cells that can mediate airway inflammation and hyperresponsiveness through prod

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

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

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

124 0.0001), resulting in significantly reduced airway inflammation and improved Pseudomonas clearance (

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

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

127 els of house dust mite- or ovalbumin-induced airway inflammation and influenza A virus or Citrobacter

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

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

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

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

132 ation of type 2 cytokines induced pronounced airway inflammation and mucus metaplasia in WT mice, whi

133 Asthma is a syndrome characterized by airway inflammation and obstruction.

134 sease (crystal-induced peritonitis, allergic airway inflammation and psoriasis), we found that target

135 The constellation of findings includes airway inflammation and rapid development of pulmonary e

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

137 tudy aimed to determine the role of Hsp70 in airway inflammation and remodeling using a mouse model o

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

139 vere uncontrolled asthma, but its effects on airway inflammation and remodelling are unknown.

140 eterogeneity exists regarding the pattern of airway inflammation and response to treatment, prompting

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

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

143 revented house dust mite-driven eosinophilic airway inflammation and significantly reduced Th2 cytoki

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

145 ter and photocopier emissions (LPEs) induces airway inflammation and systemic oxidative stress, cytot

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

147 Studies comparing airway inflammation and the airway microbiome are sparse

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

149 artly via effects of intermittent hypoxia on airway inflammation and tissue remodeling.

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

151 hma development, asthma exacerbation, and/or airway inflammation and to determine the timing of vitam

152 c potential of MIS416 in A alternata-induced airway inflammation and validated these findings in huma

153 he development of allergen-induced asthmatic airway inflammation and which immune modulating mechanis

154 terial infection, predisposition to allergic airway inflammation, and development of immune cell popu

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

156 , usually with a severe course, eosinophilic airway inflammation, and increased production of pro-inf

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

158 type 2 cytokine-induced signal transduction, airway inflammation, and mucus metaplasia in the lungs.

159 ivator of transcription 6 (STAT6) signaling, airway inflammation, and mucus metaplasia were assessed.

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

161 Bronchial hyperreactivity, airway inflammation, and sensitization were significantl

162 Blimp-1-deficient mice, a model of allergic airway inflammation, and T-cell adoptive transfer to rec

163 with thymic stromal lymphopoietin (TSLP), in airway inflammation, antiviral activity, and lung functi

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

165 Aspects of airway inflammation are also linked to a common genetic

166 ST2(+) Treg cells in the context of allergic airway inflammation are Blimp1 dependent, express type 2

167 diverse immunologic perturbations that drive airway inflammation are consistent with clinical traits

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

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

170 e recombinant Asp t 36 was able to stimulate airway inflammation, as demonstrated by an influx of eos

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

172 During allergic airway inflammation, Bcl6 and Blimp1 play dual roles in

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

174 gest that Tet1 inhibits HDM-induced allergic airway inflammation by direct regulation of the IFN and

175 is critical to induction of asthma/allergic airway inflammation by driving type 2 inflammatory respo

176 that SP-A aids in the resolution of allergic airway inflammation by promoting eosinophil clearance fr

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

178 L-33 enhanced airway hyperresponsiveness and airway inflammation by suppressing innate and adaptive a

179 the lipopolysaccharide-induced rat model of airway inflammation by the inhaled route.

180 Differences in airway inflammation can contribute to diminished asthma

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

182 l IL-6TS activation in the absence of type 2 airway inflammation defines a novel subset of asthmatic

183 r to the forefront of the pathophysiology of airway inflammation, different approaches to diagnose an

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

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

186 f epithelial expression of versican promotes airway inflammation during RSV infection further demonst

187 however, whether these factors contribute to airway inflammation during RSV infection remains unknown

188 were crucial for the development of AHR and airway inflammation, during RSV infection.

189 nting three different phenotypes of allergic airway inflammation-eosinophilic, mixed, and neutrophili

190 While PPARG has been associated with airway inflammation, ETV4 has not yet been implicated in

191 Total airway inflammation following HDM did not differ between

192 y hyperresponsiveness and Ag-specific type 2 airway inflammation following peripheral sensitization a

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

194 Hsp70 resulted in a significant reduction in airway inflammation, goblet cell hyperplasia, and Th2 cy

195 (BM) transfer studies show that SEA-induced airway inflammation, goblet cell hyperplasia, and Th2 cy

196 S. pneumoniae, Spp1(+/+) mice with allergic airway inflammation had a significantly lower bacterial

197 However, the function of Hsp70 in allergic airway inflammation has remained largely unknown.

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

199 ican in the subepithelial space in promoting airway inflammation; however, whether these factors cont

200 a complex, chronic disease characterized by airway inflammation, hyperresponsiveness and remodelling

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

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

203 grass pollen exposure and lung function and airway inflammation in a community-based sample, and whe

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

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

206 ncurrent pneumococcal infection and allergic airway inflammation in a murine model.

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

208 th pediatric asthma development and allergic airway inflammation in animal models.

209 rks present in the sputum that contribute to airway inflammation in asthma has not been published.Obj

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

211 ST2 is required for the exacerbated allergic airway inflammation in Bcl6(fl/fl) Foxp3-Cre mice.

212 te (HDM) extract was used to induce allergic airway inflammation in both wild-type (Spp1(+/+) ) and O

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

214 me of antigen inhalation challenge inhibited airway inflammation in epicutaneously sensitized mice.

215 (3) wood smoke particles caused neutrophilic airway inflammation in human volunteers, with GSTM1 null

216 umigatus antigens can also drive exaggerated airway inflammation in humans.

217 ediator governing susceptibility to allergic airway inflammation in infant mice.

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

219 ptor-induced inflammatory genes in vitro and airway inflammation in murine models.

220 OCS3(+/+) bone marrow-derived DCs (BMDCs) on airway inflammation in ovalbumin (OVA)-sensitized asthma

221 entifies DUSP10 as an important regulator of airway inflammation in respiratory viral infection.IMPOR

222 Ly-6C(+) dendritic cells and type 2 allergic airway inflammation in response to house dust mites.

223 sociated with worse quality of life and more airway inflammation in studies 1, 2, and 3.

224 ions, with an emphasis on the role of type 2 airway inflammation in the context of acute exacerbation

225 ns (SEAs) to induce robust Th2 responses and airway inflammation in the lungs.

226 -10(+) cells dramatically decreased allergic airway inflammation in wild-type and Sema4c(-/-) mice.

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

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

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

230 ds may be beneficial in alleviating allergic airway inflammation induced by fungal allergens.

231 In a murine model of neutrophilic airway inflammation induced by HDM and polyinosinic-poly

232 Airway inflammation is a critical feature of lower respi

233 ma is a chronic respiratory disease in which airway inflammation is a key feature, even in the milder

234 en asthma, atopy, and underlying type 2 (T2) airway inflammation is complex.

235 uch as lung function changes and increase in airway inflammation is limited.

236 ntributes to M. pneumoniae- and HRV-mediated airway inflammation is poorly understood.

237 Allergic airway inflammation is triggered by allergen exposure th

238 While sex hormones regulate airway inflammation, it remained unclear whether estroge

239 Children with airway inflammation linked to aerodigestive disorder wer

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

241 mechanistic analysis of TSLP-mediated type 2 airway inflammation METHODS: To dissect the mechanisms o

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

245 ocytes were analyzed in an adoptive transfer airway inflammation mouse model in response to 9-cis ret

246 Airway inflammation, mRNA levels in the lungs, and airwa

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

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

249 s robust protective effects against allergic airway inflammation not only in first- but also second-g

250 ignaling was only sufficient to limit type 2 airway inflammation, not AHR.

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

252 e-cigarettes containing nicotine suppressed airway inflammation (p < 0.001 for all) but did not alte

253 to Room Air, nicotine-free Cinnacide reduced airway inflammation (p = 0.045) and increased peripheral

254 and in mouse models, TSLP can promote type 2 airway inflammation, primarily through the activation of

255 D feeding attenuates the development of AHR, airway inflammation, pulmonary DC recruitment and MHC-II

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

257 addition, in vivo data from a mouse model of airway inflammation reveal a protective role for NLRP1 i

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

259 myeloid cell-derived IL-33 was required for airway inflammation, ST2(+) myeloid cells contributed to

260 myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL-33

261 nza virus infection and exacerbates allergic airway inflammation susceptibility, indicating that posi

262 d migration in vitro, and in down-regulating airway inflammation, T helper 2/T helper 17 cytokine res

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

264 as an uncoupling of airway obstruction from airway inflammation that can be driven by structural cha

265 asthma (AA) is characterized as a Th2-biased airway inflammation that can develop lung inflammation a

266 use models of allergen- and bleomycin-driven airway inflammation that neutralization of the TNF famil

267 treatment targets, such as control of type-2 airway inflammation, that can be achieved with currently

268 onal signaling transduction is attributed to airway inflammation, the exact mechanism of airway remod

269 ngs such as house dust mite-induced allergic airway inflammation, the lack of IRF4 expression in the

270 Hsp70 in hematopoietic cells during allergic airway inflammation; this illustrates the potential util

271 t treatment also limited HDM-driven allergic airway inflammation through an action on alveolar macrop

272 R9 activation alleviates ILC2-driven AHR and airway inflammation through direct suppression of cell f

273 n by CpG A suppresses IL-33-mediated AHR and airway inflammation through inhibition of ILC2s.

274 phages were subjected to different models of airway inflammation to evaluate the effect of GM-CSF sig

275 DC1s did not develop Th2-driven eosinophilic airway inflammation upon HDM exposure, but rather showed

276 xamined the role of BDNF in allergen-induced airway inflammation using 2 transgenic models: 1) tropom

277 We measured airway inflammation using immunofluorescence, leukocyte

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

279 athway licenses the Th2 response in allergic airway inflammation via promoting lymph node egress.

280 Airway inflammation was assessed by fractional exhaled n

281 House dust mite-induced airway inflammation was assessed by using a complete Gim

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

283 Allergen-driven airway inflammation was assessed in a mouse model of acu

284 Allergic airway inflammation was assessed in vivo in an ovalbumin

285 Importantly, airway inflammation was associated with impaired percept

286 For Studies 1 and 2, airway inflammation was measured based on sputum differe

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

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

289 d functional characteristics, and markers of airway inflammation were analyzed in an international, m

290 airway hyperresponsiveness and eosinophilic airway inflammation were both completely diminished, and

291 airway hyperresponsiveness and eosinophilic airway inflammation were both significantly attenuated,

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

293 a preclinical mouse model of acute allergic airway inflammation when administered at the time of all

294 ventional T cells, strongly promote allergic airway inflammation when transferred into recipient mice

295 A Th2 immune response is central to allergic airway inflammation, which afflicts millions worldwide.

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

297 llenge, CD-fed mice developed strong AHR and airway inflammation, which were markedly reduced in HFD-

298 reating cystic fibrosis (CF) airway disease, airway inflammation with associated mucociliary dysfunct

299 (p = 0.049), with a trend towards increased airway inflammation with nicotine-free Black Licorice ex

300 and were also characterized by eosinophilic airway inflammation, yet increased production of pro- (L