ライフサイエンスコーパス: airway remodeling

1 irway inflammation, hyperresponsiveness, and airway remodeling.

2 d elastance), eosinophilic inflammation, and airway remodeling.

3 can express factors that drive subepithelial airway remodeling.

4 ogression of morphologic emphysema and small airway remodeling.

5 ing its salutary effects on fibrinolysis and airway remodeling.

6 duration) and the development of subsequent airway remodeling.

7 grity, diminished lung function and impaired airway remodeling.

8 HT may be targeted to prevent asthma-related airway remodeling.

9 luated for cellular features associated with airway remodeling.

10 mice were protected from D. farinae-induced airway remodeling.

11 s of eosinophilic inflammation and levels of airway remodeling.

12 d which may play a key role in mechanisms of airway remodeling.

13 ration in airway smooth muscle function, and airway remodeling.

14 ry and profibrotic agents that contribute to airway remodeling.

15 tion, TGF-beta1 and collagen expression, and airway remodeling.

16 te and chronic lung diseases associated with airway remodeling.

17 , allergic and nonallergic inflammation, and airway remodeling.

18 e immunodeficient and display increased lung airway remodeling.

19 F-beta and thereby ameliorating pathological airway remodeling.

20 that modify the immune response and trigger airway remodeling.

21 ines are neutralized to define their role in airway remodeling.

22 ressing TGF-beta1 to the airway and enhanced airway remodeling.

23 al derived NF-kappaB regulated chemokines in airway remodeling.

24 consistent pathologic component of asthmatic airway remodeling.

25 enes that may contribute to allergen-induced airway remodeling.

26 pithelial chimerism was also associated with airway remodeling.

27 peribronchiolar inflammation, and structural airway remodeling.

28 eased by day 14 p.i. and was associated with airway remodeling.

29 5, eosinophils, alphaVbeta6, and TGF-beta in airway remodeling.

30 ory cells, cytokine signatures, and fibrotic airway remodeling.

31 scin reflects disease activity in asthma and airway remodeling.

32 SV lower respiratory tract infection-induced airway remodeling.

33 Asthma is associated with airway remodeling.

34 unologic (busulfan) method, markedly reduced airway remodeling.

35 ween allergic inflammation and initiation of airway remodeling.

36 ve profound effects on ASM cell function and airway remodeling.

37 d/or parenchymal changes as well as proximal airway remodeling.

38 that impairment of this function may augment airway remodeling.

39 el therapeutic approach in the management of airway remodeling.

40 obacco smoke exposure on lung parenchyma and airway remodeling.

41 landin E2 synthesis has been associated with airway remodeling.

42 ey have not been shown to directly influence airway remodeling.

43 ronchoconstriction, airway inflammation, and airway remodeling.

44 response, and SEMA3D has a plausible role in airway remodeling.

45 asthma is characterized by inflammation and airway remodeling.

46 to corticosteroid therapy and show increased airway remodeling.

47 a before the development of inflammation and airway remodeling.

48 ensitivity, the epithelial cell profile, and airway remodeling.

49 oodborne progenitor cells may participate in airway remodeling.

50 man lung fibroblasts (HLFs) is implicated in airway remodeling.

51 ation, airway hyperresponsiveness (AHR), and airway remodeling.

52 rotein YKL-40 has been related to asthma and airway remodeling.

53 to allergic inflammation, AHR, and fibrotic airway remodeling.

54 are cardinal features of asthma and initiate airway remodeling.

55 ctoside-binding lectin galectin-3 (Gal-3) in airway remodeling, a characteristic feature of asthma th

56 matrix deposition and fibrosis in asthmatic airways remodeling, a pathologic process still without e

57 We sought to compare QCT parameters of airway remodeling, air trapping, and emphysema between a

58 Computed tomography (CT)-assessed proximal airway remodeling and air trapping in asthmatic patients

59 ammatory response to ovalbumin from those of airway remodeling and airway hyperresponsiveness, illust

60 tly cited as important for the mechanisms of airway remodeling and airway hyperresponsiveness.

61 highlighted in the section on asthma include airway remodeling and anti-inflammatory therapy, leukotr

62 expression in the airway and contributes to airway remodeling and asthma severity.

63 e to inflammation, adversely effecting lower airway remodeling and asthma severity.

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

65 by enzyme-linked immunosorbent assay, while airway remodeling and cytokine production were studied b

66 Airway remodeling and emphysema were determined morphome

67 thout PH and to correlate CT measurements of airway remodeling and emphysema with PH.

68 lecular targets for the treatment of chronic airway remodeling and fibrosis in asthma.

69 ared biological roles of ORMDLs, influencing airway remodeling and hyperresponsiveness.

70 However, airway remodeling and inflammation have not been extensi

71 wall thickness (WT-Pi10) was used to assess airway remodeling and low lung area percentage (LAA%) to

72 pletion and corticosteroid administration on airway remodeling and lung function were examined.

73 Induction in the mature lung caused airway remodeling and peribronchiolar nodules, but alveo

74 considerable evidence of lesion healing and airway remodeling and reestablishment.

75 airway hyperresponsiveness, but its role in airway remodeling and steroid resistance is unknown.

76 zing antibodies to SCF significantly reduced airway remodeling and suppressed the recruitment of thes

77 lavage eosinophil composition and suppressed airway remodeling and T cell migration into the lung in

78 tered as anti-inflammatory therapy may favor airway remodeling and therefore be detrimental.

79 e to stop progression of emphysema and small airway remodeling and to partially protect against pulmo

80 unique role for TRPV4 in D. farinae-induced airway remodeling and warrant further studies in humans

81 The latter has worse small airways remodeling and narrowing, which account for the

82 ithelium, leading to allergic sensitization, airway remodeling, and eosinophilic inflammation in mous

83 eness (AHR), reversible airflow obstruction, airway remodeling, and episodic exacerbations caused by

84 tamin D are associated with asthma severity, airway remodeling, and exacerbation rate increase, espec

85 bs (e.g., IgG1, IgE, and IgA), eosinophilia, airway remodeling, and hyperresponsiveness; all pathophy

86 way increase expression of genes relevant to airway remodeling, and increase the collagen synthesis o

87 neutrophilic and eosinophilic inflammation, airway remodeling, and lung expression of several cytoki

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

89 Epithelial damage and airway remodeling are consistent features of bronchial a

90 is diagnosed, eosinophilic inflammation and airway remodeling are established in the bronchial airwa

91 ucus metaplasia, subepithelial fibrosis, and airway remodeling are significantly augmented.

92 Inflammation and airway remodeling are two responses readily apparent in

93 c airway inflammation and fibrosis, known as airway remodeling, are defining features of chronic obst

94 ctural alterations, variously referred to as airway remodeling, are well documented in the asthmatic

95 tional endotoxin exposure to parenchymal and airway remodeling as defined by quantitative computed to

96 c stem cells, is important in the process of airway remodeling as well.

97 3 signaling is required for allergen-induced airway remodeling, as well as allergen-induced accumulat

98 smooth muscle (ASM) cells may contribute to airway remodeling associated with asthma.

99 hat adaptive T cell immunity is required for airway remodeling because mice deficient in alpha/beta T

100 Airway remodeling burden is not limited to airflow limit

101 that eosinophils contribute substantially to airway remodeling but are not obligatory for allergen-in

102 ay inflammation, goblet cell metaplasia, and airway remodeling, but all of these features in this vir

103 Angiogenesis is a consistent feature of airway remodeling, but its contribution to pathophysiolo

104 Finally, Lyn may critically regulate airway remodeling by directly interacting with TGF-beta3

105 may play an important role in the process of airway remodeling by promoting the proliferation of airw

106 nterleukin-31 may play a significant role in airway remodeling by promoting the recruitment of bone m

107 This allergen-induced airway remodeling can be replicated in a mouse asthma mo

108 sistent asthma and asthma exacerbations; (3) airway remodeling: clinical consequences and reversibili

109 antification of emphysema, CT measurement of airway remodeling correlates with PAPm and could be used

110 onary disease (COPD) that has developed from airway remodeling due to asthma, as compared with other

111 Contributions of mechanical signals to airway remodeling during asthma are poorly understood.

112 nophils and suggest a potential mechanism of airway remodeling during chronic disease.

113 iferation of ASM directly contributes to the airway remodeling during development of lung diseases su

114 chronic inflammation, mucus hypersecretion, airway remodeling, emphysema, and reduced lung function.

115 Thoracic imaging provides a way to quantify airway remodeling, emphysematous destruction, regional v

116 chial T-cell and eosinophil accumulation and airway-remodeling features, such as goblet cell hyperpla

117 d airway remodeling, mice that had developed airway remodeling following 3 mo of repetitive OVA chall

118 the respiratory epithelium and the degree of airway remodeling following alloimmune injury.

119 ASM cell growth and migration that occur in airway remodeling found in asthma and chronic obstructiv

120 this deficit occurs first or is secondary to airway remodeling has been unclear.

121 way inflammation/hyperreactivity and chronic airway remodeling/hyperreactivity phenotypes (the latter

122 To determine the role of IL-5 in airway remodeling, IL-5-deficient and WT mice were sensi

123 way hyperresponsiveness in 4 wk, followed by airway remodeling in 8 wk.

124 dy goal was to determine whether established airway remodeling in a mouse asthma model is reversible

125 eculate that this response may contribute to airway remodeling in allergic inflammation.

126 mmunity; and the development of fibrosis and airway remodeling in animal models of lung injury and al

127 onchiolar fibrosis is a prominent feature of airway remodeling in asthma and involves fibroblast grow

128 nse and indicate that factor Xa functions in airway remodeling in asthma by stimulating mucin product

129 However, the contribution of ETS to airway remodeling in asthma is at present unknown.

130 Airway remodeling in asthma is defined by several struct

131 ooth muscle (ASM) is an important feature of airway remodeling in asthma that is characterized by enh

132 e marrow-derived fibroblasts are involved in airway remodeling in asthma, but the role and mechanism

133 The ATF6 target gene SERCA2b, implicated in airway remodeling in asthma, was strongly induced in the

134 x, and vascularity are prominent features of airway remodeling in asthma, whereas the extent of such

135 a T-helper 2 cytokine, is a key mediator of airway remodeling in asthma, yet the mechanism through w

136 el FABP4 as a potential target of pathologic airway remodeling in asthma.

137 ion of SERCA2b, which has been implicated in airway remodeling in asthma.

138 e-9 is implicated in airway inflammation and airway remodeling in asthma.

139 and goblet cell hyperplasia consistent with airway remodeling in asthma.

140 ersistent symptoms but may reduce aspects of airway remodeling in asthma.

141 hypertrophy and hyperplasia, contributing to airway remodeling in asthma.

142 IL-13 is a key cytokine involved in airway remodeling in asthma.

143 ed in the pursuit of therapeutic options for airway remodeling in asthma.

144 ration and migration are major components of airway remodeling in asthma.

145 fibronectin are major pathologic features of airway remodeling in asthma.

146 actor Ets-1, and suggest a role for Ets-1 in airway remodeling in asthma.

147 They may be effective in reducing airway remodeling in asthma.

148 rtant mechanism postulated to play a role in airway remodeling in asthma.

149 they may play a role in the pathogenesis of airway remodeling in asthma.

150 tribute to the initiation and progression of airway remodeling in asthmatic patients by recruiting fi

151 fore might contribute to the pathogenesis of airway remodeling in asthmatic patients.

152 tory cell migration, DP2 might contribute to airway remodeling in asthmatic patients.

153 argeting PVT1 might be effective in reducing airway remodeling in asthmatic patients.

154 TGF-beta1 is thought to play a role in airway remodeling in asthmatic subjects.

155 mediate the effects of TGF-beta1 and promote airway remodeling in children with severe asthma.

156 PAR2 prevents allergic inflammation, AHR and airway remodeling in chronic allergic airway inflammatio

157 he current literature emphasizes the role of airway remodeling in chronic persistent asthma and its p

158 There is a lack of proximal airway remodeling in cluster 2 subjects.

159 abnormalities, gas trapping, emphysema, and airway remodeling in COPD.

160 duction in peripheral blood eosinophilia and airway remodeling in CpG-ODN-treated mice emphasized its

161 esis of these alterations, the importance of airway remodeling in generating the asthma phenotype, an

162 ogic analysis of the lung showed evidence of airway remodeling in mice exposed to HDM, with goblet ce

163 scle (ASM) mass is an essential component of airway remodeling in patients with severe asthma, yet th

164 tudy to evaluate the effect of gallopamil on airway remodeling in patients with severe asthma.

165 ely steroid-resistant mediator that promotes airway remodeling in patients with STRA and is an import

166 vestigate the relationship between IL-33 and airway remodeling in pediatric patients with STRA.

167 trate an enhanced risk of emphysema or small airway remodeling in response to cigarette smoke.

168 scle (BSM) mass, a characteristic feature of airway remodeling in severe asthma, is associated with r

169 uscle hypertrophy is one of the hallmarks of airway remodeling in severe asthma.

170 Studies of allergen induced airway remodeling in transgenic mice suggest an importan

171 The higher degree of airway remodeling in WT mice was associated with higher

172 icantly increases levels of allergen-induced airway remodeling (in particular smooth muscle thickness

173 nophilic airway inflammation and features of airway remodeling, in particular subepithelial fibrosis,

174 Important pathologic components of airway remodeling include fibrosis and abnormal innate a

175 y epithelial damage and hyperreactivity, and airway remodeling including smooth muscle hyperplasia an

176 TAS2R agonists attenuated features of airway remodeling including smooth muscle mass, extracel

177 ys a central role in bronchoconstriction and airway remodeling, including airway smooth muscle growth

178 tracts induced a severe phenotype of chronic airway remodeling, including exacerbated mucus productio

179 siveness and reduced several key features of airway remodeling, including goblet cell hyperplasia and

180 mice have significantly increased levels of airway remodeling, including increased airway smooth mus

181 nes in airway epithelium in allergen-induced airway remodeling, including peribronchial fibrosis and

182 hat computed tomographic (CT) measurement of airway remodeling instead of emphysema may correlate wit

183 Airway remodeling is a detrimental and refractory proces

184 Airway remodeling is a prominent feature of certain immu

185 Chronic airway remodeling is a serious consequence of asthma, wh

186 Asthma airway remodeling is linked to Th2 inflammation.

187 mice had significantly increased markers of airway remodeling like collagen deposition.

188 thus, mechanisms other than inflammation and airway remodeling may be involved in the pathogenesis of

189 Thus, pathways leading to certain aspects of airway remodeling may not depend on leukocyte recruitmen

190 ing YKL-40 levels (r=0.55, P<0.001) and with airway remodeling (measured as the thickness of the sube

191 quences of DNA (ISS) can reverse established airway remodeling, mice that had developed airway remode

192 Airway remodeling might explain lung function decline am

193 Naphthalene-induced airway remodeling nonsignificantly increased the number

194 t that PAI-1 could play an important role in airway remodeling of asthma, and inhibition of PAI-1 act

195 increased airway smooth muscle mass seen in airway remodeling of patients with severe asthma.

196 of life caused alveolar enlargement without airway remodeling or peribronchiolar nodules.

197 ignificant eosinophilic airway inflammation, airway remodeling, or increased airway hyperreactivity t

198 e dependent (large alveoli) and independent (airway remodeling, peribronchiolar nodules) of lung grow

199 role for altered ECM production in asthmatic airway remodeling, possibly regulated by unbalanced AEC

200 is a key determinant in the control of lower airway remodeling posttransplantation.

201 at ORMDL3 plays an important role in vivo in airway remodeling potentially through ATF6 target genes

202 Increased levels of airway remodeling preceded increased levels of airway in

203 the magnitude of airway hyperreactivity and airways remodeling produced in nonhuman primates with ex

204 -kappaB in allergen-induced inflammation and airway remodeling remains unclear.

205 satile functions, the role of Lyn in chronic airway remodeling remains undefined.

206 asthma phenotype, and the natural history of airway remodeling responses have not been adequately def

207 rate that CCR1 is a major contributor to the airway remodeling responses that arise from A. fumigatus

208 ining the reversibility of transgene-induced airway remodeling responses.

209 terleukin 11 (IL-11) and IL-13 might make to airway remodeling responses.

210 s associated with eosinophil recruitment and airway remodeling revealed that levels of eotaxin-1, IL-

211 c phenotype (airways hyperresponsiveness and airways remodeling), rhesus monkeys with experimentally

212 to mechanical stress mimics key features of airway remodeling seen in asthma: namely, an increase in

213 provide new therapeutic approaches to alter airway remodeling seen in patients with chronic airflow

214 mice that had already developed established airway remodeling significantly reduced the degree of ai

215 rmine the role of Smad 3 in allergen-induced airway remodeling, Smad 3-deficient and wild-type (WT) m

216 evels of expression of genes associated with airway remodeling (TGF-beta1, ADAM8) were detected in ai

217 reased expression of genes important to both airway remodeling [TGF-beta1, 5-lipoxygenase (5-LO)] and

218 re to OVA allergen induces greater levels of airway remodeling than exposure to either chronic ETS or

219 smooth muscle (BSM) mass is a key feature of airway remodeling that classically distinguishes severe

220 The irreversible airway remodeling that occurs in asthma has been attribu

221 the adaptive immune system is essential for airway remodeling that occurs in mice that are chronical

222 tissues from asthmatic subjects with severe airway remodeling that was similar to that seen in the I

223 heir importance is unknown in the context of airway remodeling, their involvement in atherosclerosis

224 have used a mouse model of allergen-induced airway remodeling to determine whether the combination o

225 a wide range of studies, including those on airway remodeling, transepithelial transport and inflamm

226 evaluated as markers of activation of upper airway remodeling using image analysis, together with re

227 4 regulates Dermatophagoides farinae-induced airway remodeling via 2 distinct pathways modulating mat

228 t Gal-3 is an important lectin that promotes airway remodeling via airway recruitment of inflammatory

229 Airway remodeling was analyzed at baseline and after tre

230 This increased airway remodeling was associated with selective activati

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

232 Vascular and airway remodeling, which are characterized by airway smo

233 Prolonged inflammation may lead to airway remodeling, which can result in physiologic abnor

234 xious environmental stimuli that can trigger airway remodeling, which contributes significantly to ai

235 mechanisms responsible for the initiation of airway remodeling, which contributes to decreased lung f

236 ta3 isoform and modulates the development of airway remodeling, which may have therapeutic implicatio

237 nd T cell-predominant inflammatory response, airway remodeling with increased types III and I collage

238 mononuclear cell infiltrates and impressive airways remodeling with subepithelial fibrosis.

239 HR and a significant spontaneous increase in airway remodeling, with increased smooth muscle mass and

240 hma is previously unknown, regulates AHR and airway remodeling without airway inflammation through a