ライフサイエンスコーパス: airway

1 rapped in a layer of mucous out of the upper airway.

2 ls can enter the lung parenchymal tissue and airway.

3 ed microbiome of the mucosal surfaces of the airways.

4 vement beyond mere colonization of the upper airways.

5 o cytokines or natural allergens through the airways.

6 hils and proneutrophilic biomolecules in the airways.

7 , and increased CD8(+) T cell numbers in the airways.

8 t occasionally colonize and infect the human airways.

9 lymphocyte activation and migration into the airways.

10 barrier function in 16HBE cells and in mouse airways.

11 an ideal system for studying B cells in the airways.

12 CD8+ T, NKT-like, and NK cells in the small airways.

13 In the airway, 15-epi LXA4 production is stimulated by the epit

14 /expiratory CTs to identify functional small airway abnormality (PRM(FSA)) and emphysema (PRM(EMPH))

15 ous exacerbations, greater evidence of small airway abnormality on CT, lower interleukin-15 concentra

16 very of an alpha5beta1 inhibitor into murine airways abrogated the exaggerated bronchoconstriction in

17 It is not known how DEP exposure activates airway afferents to elicit symptoms, such as cough and b

18 py to prevent the progression of Ova induced airway allergy in mice.

19 -2 deficiency led to exacerbated HDM-induced airway allergy, with increased airway and tissue eosinop

20 ronal signalling, smooth muscle contraction, airway and exocrine gland secretion, and rhythmic moveme

21 d HDM-induced airway allergy, with increased airway and tissue eosinophilia, lung inflammation, and I

22 the two adult lung epithelial compartments (airways and alveoli) are separately maintained by distin

23 vironmentally derived chitin polymers in the airways and expression of pro-fibrotic cytokines.

24 llergen exposure on TREM-2 expression in the airways and on DC subsets in the lung and lymph nodes in

25 nflammation in the lungs that constricts the airways and presents as coughing and wheezing.

26 Protease-activated receptor 2 activates airway apical membrane chloride permeability and increas

27 hanges and altered the proteomic profiles of airway apical secretions compared to cigarette-exposed H

28 an organism frequently colonizing the upper airways, at the human mucosal site of the disease.

29 t been conducted, particularly in a relevant airway background using a functional readout.

30 Primary human airway basal stem cell-derived epithelial cultures and m

31 rgic asthmatics, but it is unclear what role airway basophils play in "TH2-low" asthma phenotypes.

32 s representative of the trachea versus small airway bronchiolar cells.

33 lar lavage, large proximal, and small distal airway brushings were collected from patients with BOS (

34 tratracheal administration of DEPs activated airway C-fibers.

35 End expiratory pressure dependent changes in airway caliber and recruitment were estimated from mecha

36 Replication kinetics in human airway cells and pathogenesis and transmissibility in an

37 response and its interactions with resident airway cells is critical to advancing knowledge on asthm

38 ent inhibited MERS-CoV entry of Calu-3 human airway cells, thus providing direct evidence that virus-

39 ing were analyzed in allergen-sensitized and airway-challenged mice.

40 In this article, we show that airway challenges with the parent CysLT, leukotriene C4

41 B was defined as a presence of chronic upper airway complications.

42 The extent of this airway contraction is proportional to the frequency of C

43 of ciliary beating, is the primary physical airway defense against inhaled pathogens and irritants.

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

45 nduced, severe, steroid-insensitive allergic airway disease (SSIAAD) in BALB/c mice were developed an

46 Asthma is a chronic airway disease characterized by inflammation, mucus hype

47 the IL-1R family genes was validated in the Airway Disease Endotyping for Personalized Therapeutics

48 49d to drive development of postviral atopic airway disease in mice.

49 isplay infertility as well as severe chronic airway disease leading to postnatal death.

50 transfer studies in mouse models of allergic airway disease, we examined the effects of Act-A-iTreg c

51 ts and NOX inhibitors in mitigating allergic airway disease.

52 eptors in the lung protects against allergic airway disease.

53 of distal lung ventilation reflecting small-airway disease.

54 g component, referred to as functional small airways disease (fSAD).

55 linked mechanistically in models of allergic airways disease and have been associated with asthma sev

56 The Airways Disease Endotyping for Personalized Therapeutics

57 en proposed as "treatable traits" in chronic airways disease, adding impetus to their evaluation and

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

59 uced glycolysis and pathogenesis of allergic airways disease.

60 Use of inhalants for obstructive airway diseases (PR = 0.79; 95% CI = 0.74-0.85) also dec

61 elated conditions, inhalants for obstructive airway diseases and glucocorticoid use.

62 (TRAP) exposure is associated with allergic airway diseases and reduced lung function in children, b

63 of human conditions associated with chronic airway diseases, hydrocephalus and infertility.

64 Neutrophilic airway diseases, including cystic fibrosis, are characte

65 ance to increase the awareness towards upper airway disorders in the swimming athletes and to ensure

66 (-/-) swine, suggesting that cystic fibrosis airways do not respond to inhaled pathogens, thus favori

67 n alveolar macrophage cells in the lungs and airways, early induction of virus specific antibodies, r

68 splanted myofascial flap was analyzed in the airway environment.

69 sinophil numbers but had a limited effect on airway eosinophil activation markers, suggesting that th

70 Mepolizumab reduced airway eosinophil numbers but had a limited effect on ai

71 inflammation, as characterized by increased airway eosinophilia, goblet cell metaplasia, accumulatio

72 rved in subjects with elevated serum IgE and airway eosinophilia.

73 at infects well-differentiated primary human airway epithelia (HAE) in vitro In human embryonic kidne

74 apical surface of well-differentiated human airway epithelia (HAE).

75 st study investigating the effect of AMPs on airway-epithelia associated genes upon administration to

76 laudin-18 is an essential contributor to the airway epithelial barrier to aeroantigens.

77 Claudin-18.1 mRNA levels were measured in airway epithelial brushings from healthy controls and pa

78 of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid

79 dexamethasone to modulate gene expression in airway epithelial cells coincided with its potency to re

80 ed interferon response to viral infection by airway epithelial cells may be a mechanism leading to lu

81 so used to reconstitute ORMDL3 expression in airway epithelial cells of Ormdl3 knockout mice.

82 Together, these results suggest beta2ARs on airway epithelial cells promote the asthma phenotype and

83 IL-13 levels were increased in airway epithelial cells, macrophages, type 2 innate lymp

84 g this innate immune response in human small airway epithelial cells.

85 sm of a discrete population of multiciliated airway epithelial cells.

86 2 strain three times in differentiated swine airway epithelial cells.

87 her microorganisms and form EETs at sites of airway epithelial damage to protect the host from infect

88 In human airway epithelium air-liquid interface (HAE-ALI) culture

89 Integrity of the airway epithelium is essential for normal lung function.

90 e, transgenic expression of beta2ARs only in airway epithelium is sufficient to rescue IL-13-induced

91 along with increased Il33 expression in the airway epithelium of Scnn1b-Tg mice.

92 of lactate dehydrogenase A occurring in the airway epithelium.

93 shows the receptors are highly expressed in airway epithelium.

94 SM impair barrier function in differentiated airway epithelium.

95 mucosa; proliferation of goblet cells in the airway epithelium; and the production of antigen-specifi

96 curring in the upper airway may mirror lower airway events.

97 increased bacterial survival in CFA-exposed airway explants, ASL, and AMPs.

98 disease and neutrophilic infiltration of the airways, features more usually associated with severe as

99 lness is not innocuous but may determine the airway function of these subjects by driving immune cell

100 Airway goblet cell differentiation and related mucus ove

101 The upper airways have been shown to reflect colonization of the l

102 wheeze and presence of airflow limitation or airway hyper-reactivity, or both).

103 5 and IL-13), serum immunoglobulin (Ig)E and airway hyper-responsiveness (AHR).

104 ice gavaged with purified R gnavus developed airway hyper-responsiveness and had histologic evidence

105 ial target for new bronchodilators to reduce airway hyper-responsiveness in asthma.

106 role for smooth muscle ARHGEF1 in asthmatic airway hyper-responsiveness is worthy of further investi

107 h muscle (ASM) axis that underlies prolonged airway hyperreactivity (AHR) in mice.

108 pa-deficient mice did not experience AAI and airway hyperreactivity.

109 lic and neutrophilic airway inflammation and airway hyperresponsiveness (AHR) following allergen chal

110 r Aspergillus fumigatus (AF) extract-induced airway hyperresponsiveness (AHR), airway inflammation, i

111 isease characterized by airflow obstruction, airway hyperresponsiveness (AHR), and airway inflammatio

112 ng with an aerosolized antagonist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammat

113 of type 2-related inflammation and change in airway hyperresponsiveness after 6 weeks of fluticasone

114 tly suppressed RSV-induced steroid-resistant airway hyperresponsiveness and airway inflammation.

115 posure to Neu5Gc in mice resulted in reduced airway hyperresponsiveness and inflammatory cell recruit

116 prerequisite for the suppression of AAI and airway hyperresponsiveness by GCs.

117 d TH2 cells, type 2 cytokine production, and airway hyperresponsiveness compared with sole DEPs or HD

118 rway hyperresponsiveness; however, at 7 days airway hyperresponsiveness had completely resolved in Da

119 nt randomization, imatinib treatment reduced airway hyperresponsiveness to a greater extent than did

120 ltration, excessive Th2 polarization, marked airway hyperresponsiveness, alveolar simplification, dec

121 haracterized by variable airway obstruction, airway hyperresponsiveness, and airway inflammation.

122 V-induced mucous metaplasia, ILC2 expansion, airway hyperresponsiveness, and epithelial cell IL-25 ex

123 C2 numbers, TH2 cell numbers and activation, airway hyperresponsiveness, and expression of the transc

124 The effect of IL-17A on IL-13-induced airway hyperresponsiveness, gene expression, mucus hyper

125 c mice results in a dramatic upregulation of airway hyperresponsiveness, lung resistance, and TH2 res

126 ce results in increased lung granulocytosis, airway hyperresponsiveness, mucus overproduction, collag

127 se exposed to IL-13 and IL-17A had augmented airway hyperresponsiveness, mucus production, airway inf

128 At 24 hours, Darc(E2) mice had increased airway hyperresponsiveness; however, at 7 days airway hy

129 ptimal concentration, recovery and purity of airway immune cells from a large volume of diluent, whic

130 ungs and in affecting previously established airway immunologic tolerance.

131 n-rich extracellular matrix in the asthmatic airway in an ADAM8-dependent manner, making ADAM8 a poss

132 es a TH2-biased inflammatory response in the airways in an IL-33-dependent but TRL4-independent manne

133 elling has been long identified in the lower airways in asthma and is characterized by epithelial she

134 of a mouse colon, a rat esophagus, and small airways in sheep.

135 In cystic fibrosis (CF) patients, chronic airway infection by Pseudomonas leads to progressive lun

136 Chronic airway infections by the opportunistic pathogen Pseudomo

137 ion of these subjects by driving immune cell airway infiltration, cellular remodeling, and alteration

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

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

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

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

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

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

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

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

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

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

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

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

150 Studies comparing airway inflammation and the airway microbiome are sparse

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

152 Differences in airway inflammation can contribute to diminished asthma

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

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

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

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

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

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

159 -10(+) cells dramatically decreased allergic airway inflammation in wild-type and Sema4c(-/-) mice.

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

161 Allergic airway inflammation is triggered by allergen exposure th

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

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

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

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

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

167 Bronchial hyperreactivity, airway inflammation, and sensitization were significantl

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

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

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

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

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

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

174 losely related to the degree of eosinophilic airway inflammation.

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

176 central immune modulator promoting allergic airway inflammation.

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

178 oid-resistant airway hyperresponsiveness and airway inflammation.

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

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

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

182 imit ILC2 activation and subsequent allergic airway inflammation.

183 failed to confer protection against AHR and airway inflammation.

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

185 obstruction, airway hyperresponsiveness, and airway inflammation.

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

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

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

189 atic stable asthma and relate composition to airway inflammatory phenotype and other phenotypic chara

190 AAD was ascertained by examining changes in airway inflammatory responses, Th2 responses, and lung h

191 el can also be used to assess the effects of airway insults, including coinfections by recognized res

192 esis is that immunosuppressives might affect airway integrity.

193 The mucosal layer of conducting airways is the primary tissue exposed to inhaled microor

194 onstrated that innate immune cells (notably, airway macrophages) play essential roles in the generati

195 Congenital pulmonary airway malformation (CPAM) is a relatively rare congenit

196 at disease mechanisms occurring in the upper airway may mirror lower airway events.

197 rmine the relations among the nasopharyngeal airway metabolome profiles, microbiome profiles, and sev

198 Neutrophilic asthma is associated with airway microbiology that is significantly different from

199 tudies comparing airway inflammation and the airway microbiome are sparse, especially in subjects not

200 Manipulation of the airway microbiome, particularly in early life, might be

201 We aimed to characterize the airway microbiota in patients with symptomatic stable as

202 The one airway model proposes that disease mechanisms occurring

203 veins lacking (Vvl) largely ameliorates the airway morphogenesis defects of grh mutants.

204 Airway mucin concentrations may quantitate a key compone

205 value and 87% negative predictive value for airway mucosal CCL26-high status.

206 treatment revealed that ivacaftor decreased airway mucous plugging.

207 nstrated that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and

208 s and inflammation, but the possibility that airway nerves are dysfunctional has not been fully explo

209 ometric measurements to identify patterns of airway obstruction in children and define obstruction ph

210 IL-15 has a potent inhibitory effect on the airway obstruction that occurs in response to environmen

211 Quantifying underlying small airway obstruction via PRM(fSAD) helps further stratify

212 pacity and to markers for hyperinflation and airway obstruction were found in patients with CF.

213 ociation of the polymorphism with asthma and airway obstruction within asthmatics via multivariate lo

214 Asthma is characterized by variable airway obstruction, airway hyperresponsiveness, and airw

215 ethysmography were made preextubation during airway occlusion and on continuous positive airway press

216 of epithelial injury and inflammation in the airways of athletes was demonstrated.

217 findings suggest that MMF is present in the airways of lung transplant patients and might affect the

218 ncrease in pro-inflammatory M1s in the small airways of NLFS and COPD compared to controls with a rec

219 olyclonal" autoimmune event occurring in the airways of prednisone-dependent asthmatic patients with

220 transfer of CD3(-)NK1.1(+) NK cells into the airways of WT hosts suppressed the inflammatory response

221 Continuous positive airway pressure (CPAP) in asthma patients with concomita

222 ients who cannot tolerate continous positive airway pressure (CPAP) machines or intraoral devices.

223 apeutic decision-making, continuous positive airway pressure (CPAP) treatment or a healthy habit asse

224 asal cannula therapy and continuous positive airway pressure had similar efficacy (RR, 1.11; 95% CI,

225 ilator settings were an inspiratory positive airway pressure of 24 (IQR, 22-26) cm H2O, an expiratory

226 (IQR, 22-26) cm H2O, an expiratory positive airway pressure of 4 (IQR, 4-5) cm H2O, and a backup rat

227 airway occlusion and on continuous positive airway pressure of 5 and pressure support of 10 above po

228 the main alternative to continuous positive airway pressure, improves endothelial function in patien

229 in the duration of nasal continuous positive airway pressure.

230 cording to the protocol of Webb and Tierney (airway pressures of 14/0, 30/0, 45/10, 45/0 cm H2O).

231 s ventilatory consequences include increased airway pressures, hypercarbia, and decreased pulmonary c

232 Airways primarily secrete two closely related gel-formin

233 sponses and eosinophilic inflammation in the airways remained unaffected.

234 Securing the airway remains the most important intervention, followed

235 Airway remodeling (AR) is a prominent feature of asthma

236 retion of mucus is an important component of airway remodeling and contributes to the mucus plugs and

237 irway inflammation, hyperresponsiveness, and airway remodeling were analyzed in allergen-sensitized a

238 SV lower respiratory tract infection-induced airway remodeling.

239 landin E2 synthesis has been associated with airway remodeling.

240 The concept of upper airway remodelling has only recently been introduced, an

241 Bronchial fibroblasts play a key role in airway remodelling in asthma.

242 asthma is characterized by inflammation and airway remodelling.

243 re used to mimic a viral insult in the upper airways represented by primary human nasal epithelial ce

244 cytokines and improves allergen-induced AHR, airway resistance, and compliance.

245 ROCK2 contributes to allergic airways responses likely via effects within ASM cells an

246 Allergic airways responses were measured 48 h after the last chal

247 ROCK2 acting within CD4(+) cells in allergic airways responses.

248 tion in mucus overproduction while improving airway responsiveness to methacholine by 41%.

249 activation, airway smooth muscle growth, and airway responsiveness.

250 sessed the antimicrobial activity of exposed airway samples using both bioluminescence and standard c

251 NM myosin II plays a critical role in airway SM contraction that is independent and distinct f

252 regulated during contractile stimulation of airway SM tissues by RhoA-mediated NM myosin RLC phospho

253 h persistent airflow obstruction had greater airway smooth muscle (Asm) area with decreased periostin

254 elated mechanism along the cholinergic nerve-airway smooth muscle (ASM) axis that underlies prolonged

255 lammation, mucus hypersecretion and abnormal airway smooth muscle (ASM) contraction.

256 Activated CD4 T cells connect to airway smooth muscle cells (ASMCs) in vitro via lymphocy

257 the frequency of Ca(2+) oscillations within airway smooth muscle cells (ASMCs).

258 Airway smooth muscle cells generated pro-MMP-1, which wa

259 In airway smooth muscle cells, these Ca(2+) oscillations ar

260 ase expression was found in human and murine airway smooth muscle cells.

261 , and are preceded by long-duration waves of airway smooth muscle contraction.

262 racellular matrix, which enhanced subsequent airway smooth muscle growth by 1.5-fold (P < 0.05), whic

263 ty by transiently increasing MMP activation, airway smooth muscle growth, and airway responsiveness.

264 In asthma, mast cells are associated with airway smooth muscle growth, MMP-1 levels are associated

265 membrane thickening, subepithelial fibrosis, airway smooth muscle hyperplasia and increased angiogene

266 lpain using calpain knockout mice attenuated airway smooth muscle remodelling in mouse asthma models.

267 d cell proliferation of ASMCs and attenuated airway smooth muscle remodelling in mouse asthma models.

268 However, the role of calpain in airway smooth muscle remodelling remains unknown.

269 Airway smooth muscle treated with activated mast cell su

270 of airway inflammation, mucus, fibrosis, and airway smooth muscle were no different in Ormdl3(Delta2-

271 r regulation of RLC phosphorylation in tonic airway smooth muscle.

272 Our findings suggest that airway smooth muscle/mast cell interactions contribute t

273 sHA rapidly activated RhoA, ERK, and Akt in airway smooth-muscle cells, but only in the presence of

274 e receptor-stimulating bacteria in the upper airway (Staphylococcus aureus and Staphylococcus epiderm

275 hermore, administration of IL-1beta into the airways stimulated lactate production and expression of

276 s associated with bronchial inflammation and airway structural changes.

277 nd reversible airflow obstruction and normal airway structure.

278 MCP-3; infiltration of eosinophils into the airway submucosa; proliferation of goblet cells in the a

279 l Na(+) channel blocker amiloride, improving airway surface hydration and mucus clearance, reduced al

280 A systems-level description of airway surface liquid (ASL) homeostasis could accelerate

281 he CFTR chloride channel, leading to reduced airway surface liquid secretion.

282 fluid volume and blood pressure, as well as airway surface liquid volume and mucociliary clearance.

283 ith atopy displayed rapid induction of upper airway symptoms, an enrichment of ILC2s, eosinophils, an

284 d-type mice, led to synergistic increases in airway Th2 cytokines, eosinophilia, and peribronchial in

285 omplex formulation for siRNA delivery to the airways that consists of a liposome (DOTMA/DOPE; L), an

286 r morphologic structures and associations in airways that contain abundant submucosal glands and gobl

287 n shown to reflect colonization of the lower airways, the actual site of inflammation in asthma, whic

288 in severe asthmatics was not associated with airway tissue inflammation and remodeling, although pers

289 Using transcriptomic profiling of airway tissues, we sought to define the molecular phenot

290 mpling various compartments within the lower airways to examine human bronchial epithelial cells (HBE

291 epsis pathogen Klebsiella pneumoniae via the airways to induce pneumonia-derived sepsis.

292 he spread of viral infection from conducting airways to the alveolar epithelium is therefore a pivota

293 Airway tolerance and allergen-induced airway inflammatio

294 lood eosinophil group had slightly increased airway wall thickness (0.02 mm difference, p=0.032), hig

295 enerally high in all subjects throughout the airway wall with marked cytoplasmic to nuclear shift in

296 gh number of IFNgamma(+) CD8- T cells in the airways was associated with early viral clearance.

297 s related to medication (predominantly upper airway) was less likely.

298 enioglossus EMG and dynamic MRI of the upper airway were performed before and after administration of

299 henotypes and consistently trafficked to the airway, where they remained detectable from 6 h through

300 might affect the structural integrity of the airway, which needs further investigation and validation