ライフサイエンスコーパス: severe asthma

1 many patients, particularly those with more severe asthma.

2 iated with poor lung function in adults with severe asthma.

3 T to prevent progression from milder to more severe asthma.

4 H)17 cells, which portend the development of severe asthma.

5 nosis, targeted treatment, and monitoring of severe asthma.

6 ngly integrated into treatment strategies of severe asthma.

7 ungi such as Aspergillus fumigatus have more severe asthma.

8 analysis can contribute to the management of severe asthma.

9 ith srT2-high asthma were older and had more severe asthma.

10 tability after 12 to 18 months in those with severe asthma.

11 ic architecture between mild and moderate-to-severe asthma.

12 ping anti-tryptase as a clinical therapy for severe asthma.

13 pathogenicity of TH1 cells in patients with severe asthma.

14 elevated in moderate while downregulated in severe asthma.

15 sought to define the molecular phenotypes of severe asthma.

16 roblasts on epithelial cell proliferation in severe asthma.

17 has been shown to play an important role in severe asthma.

18 fy gene profiles associated with adult-onset severe asthma.

19 OSM-producing cells in patients with CRS and severe asthma.

20 d biologics, may be required in moderate and severe asthma.

21 e inhaled corticosteroids and 122 (31%) with severe asthma.

22 ful targets for the treatment of adult-onset severe asthma.

23 teria included eosinophilic oesophagitis and severe asthma.

24 nd radiological abnormalities in moderate to severe asthma.

25 cross the United States, including many with severe asthma.

26 ung injury were less enriched in adult-onset severe asthma.

27 ic landscape in the airways of children with severe asthma.

28 of radiological abnormalities in moderate to severe asthma.

29 lls contribute to the pathobiologic basis of severe asthma.

30 to the emergency department with moderate to severe asthma.

31 n observed in CD8 T cells from patients with severe asthma.

32 position document on the role of allergy in severe asthma.

33 evels in biopsy specimens from patients with severe asthma.

34 ontrol was maintained in adult patients with severe asthma.

35 in patients with corticosteroid-insensitive severe asthma.

36 and IL-6 release in ASMCs from patients with severe asthma.

37 the management of patients with uncontrolled severe asthma.

38 cell numbers and activation in patients with severe asthma.

39 ignificantly higher in mild while reduced in severe asthma.

40 ters 3 and 4 were dominated by patients with severe asthma.

41 mechanism driving GC insensitivity in ASM in severe asthma.

42 mily members in the bronchi of patients with severe asthma.

43 creased health care utilization, asthma, and severe asthma.

44 ntitis and P. intermedia are associated with severe asthma.

45 ival biofilm of individuals with and without severe asthma.

46 e in the proportion meeting the criteria for severe asthma.

47 ongitudinal studies whether children outgrow severe asthma.

48 ory epithelium is increased in subjects with severe asthma.

49 ee DMPs exhibited discriminatory ability for severe asthma.

50 e driven disproportionately by children with severe asthma.

51 atient clustering stability in patients with severe asthma.

52 y tended to co-occur among participants with severe asthma.

53 At baseline, 111 (59%) children had severe asthma.

54 the c-sIgE were identified as associates of severe asthma.

55 nsitized participants with mild/moderate and severe asthma.

56 prisingly also in nonallergic patients with (severe) asthma.

57 Thirty-seven children (13 with severe asthma, 8 with mild/moderate asthma, 16 age-match

58 logy, clinical diagnosis, asthma phenotypes, severe asthma, acute exacerbations, and clinical managem

59 he children with severe asthma no longer had severe asthma after 3 years; there was a stepwise decrea

60 samples were collected from 63 subjects with severe asthma and 78 subjects with moderate-to-severe CO

61 antibody (mAb) approved for the treatment of severe asthma and chronic spontaneous urticaria.

62 bodies found in the sputum of patients with severe asthma and could be a biomarker to optimize diagn

63 ment strategies are needed for patients with severe asthma and exploratory studies of unbiased nature

64 y tissue obtained from patients with mild-to-severe asthma and healthy control subjects.

65 avage fluid was collected from patients with severe asthma and healthy subjects, and the level of PTX

66 s (IL and UK) comprising mild, moderate, and severe asthma and healthy volunteers were evaluated for

67 articipants without asthma in the nonsmoking severe asthma and mild/moderate asthma subgroups were si

68 y profiled patients with mild, moderate, and severe asthma and nonatopic healthy control subjects.

69 Here we report that mice with severe asthma and OVA-sensitized/challenged mice had inc

70 fferentially expressed between patients with severe asthma and participants without asthma.

71 summary, CEACAM6 expression is increased in severe asthma and primarily associated with airway epith

72 ate in clinical assessment and management of severe asthma and some of the challenges and unmet needs

73 creased type 2 inflammation in patients with severe asthma and those with frequent exacerbations.

74 be exposed to many risk factors facilitating severe asthma and wheezing, including airborne viruses,

75 the use of different add-on medications for severe asthma, and crucially, on selection strategies.

76 safety of LAIV in children with moderate to severe asthma, and in preschool children with recurrent

77 also establishing a new-found importance in severe asthma, and in remodeling of blood vessels in can

78 genome-wide association study of moderate-to-severe asthma, and in stage 2 we followed up independent

79 ll types of asthma contribute to moderate-to-severe asthma, and provide novel mechanistic insights us

80 ed at serine 226 was increased in cells from severe asthma, and the MUC1-CT/GRalpha complex was downr

81 Treatment options are limited for severe asthma, and the need for additional therapies rem

82 ion (both with a strong gradient); diabetes; severe asthma; and various other medical conditions.

83 Patients with severe asthma appear relatively corticosteroid resistant

84 se cases; adult-onset asthma and moderate-to-severe asthma are associated with fewer genes, which are

85 ellular pathways driving the pathogenesis of severe asthma are poorly defined.

86 orticoid (GC) insensitivity in patients with severe asthma are still unknown.

87 he population was enriched for children with severe asthma, as assessed by the American Thoracic Soci

88 perresponsiveness, a physiological marker of severe asthma, as well as on airway mast-cell numbers an

89 ts relying on oral glucocorticoids to manage severe asthma associated with eosinophilia.

90 ental exposure to fungi is linked with acute severe asthma attacks, but there are few studies reporti

91 We stratified patients with moderate-to-severe asthma based on clinicophysiologic parameters and

92 ntion advises that patients with moderate to severe asthma belong to a high-risk group that is suscep

93 Poor asthma control is often driven by severe asthma biology, which has appropriately been the

94 Allergic sensitization is associated with severe asthma, but assessment of sensitization is not re

95 tory pathways are indicated to contribute to severe asthma, but their individual involvement in the d

96 ic cells has been suggested to contribute to severe asthma, but whether uptake of apoptotic cells by

97 ntify new biomolecular mechanisms underlying severe asthma by an unbiased, detailed interrogation of

98 MUC1-CT/GRalpha complex was downregulated in severe asthma cells.

99 n testing in routine clinical care within UK severe asthma centers using remote monitoring technologi

100 ith and without chronic respiratory disease (severe asthma, chronic obstructive pulmonary disease, an

101 The severe asthma clusters (T2, T3, and T4) had higher sputu

102 hage numbers were significantly decreased in severe asthma compared to mild-moderate asthma and healt

103 A(+) patients had clinical manifestations of severe asthma compared with 3 of 6 (50%) in the sputum A

104 lls and lamina propria inflammatory cells in severe asthma compared with healthy control subjects.

105 nchoalveolar lavage fluid from patients with severe asthma compared with in bronchoalveolar lavage fl

106 ulated (>2-fold) in nonsmoking patients with severe asthma compared with MMAs, including IL-1 recepto

107 eport the case of a 66-year-old patient with severe asthma complicated by eosinophilic chronic rhinos

108 stepwise decrease in the proportion meeting severe asthma criteria.

109 nd myeloid cell trafficking in patients with severe asthma, decreased B-lymphocyte development and he

110 children aged 2 to 17 years with moderate to severe asthma defined by a Pediatric Respiratory Assessm

111 sthma, as well as subgroups of patients with severe asthma defined by transcript profiles, show the v

112 present in the airways of patients who have severe asthma despite glucocorticoid treatment; these ce

113 The lower airways of children with severe asthma display a dominant TH1 signature and atypi

114 The term 'Severe Asthma' encompasses a highly heterogeneous group

115 mprovement in the management of ICU-admitted severe asthma episodes.

116 lla- cluster at YZ poses the highest risk of severe asthma exacerbation (p = 0.04).

117 nalysis comprises 2866 children experiencing severe asthma exacerbation between ages 2 and 6 years, a

118 bjects (14.7%; 95% CI, 11%-19.1%) reported a severe asthma exacerbation in the 4 weeks after immuniza

119 The primary outcome was any protocol-defined severe asthma exacerbation.

120 y outcome was time to first protocol-defined severe asthma exacerbation.

121 did not significantly improve the time to a severe asthma exacerbation.

122 The primary outcome was the time to a severe asthma exacerbation.

123 , AND PARTICIPANTS: The Vitamin D to Prevent Severe Asthma Exacerbations (VDKA) Study was a randomize

124 is model recapitulates all major features of severe asthma exacerbations and can serve to discern dri

125 librium with rs56151658 were associated with severe asthma exacerbations at a P value of .01 or less

126 Severe asthma exacerbations cause significant morbidity

127 Influenza virus triggers severe asthma exacerbations for which no adequate treatm

128 t mite-impermeable bedding and its impact on severe asthma exacerbations in children.

129 use of vitamin D3 supplementation to prevent severe asthma exacerbations in this group of patients.

130 month intervention period, the occurrence of severe asthma exacerbations was investigated.

131 al response to budesonide versus placebo for severe asthma exacerbations, lung function, and asthma s

132 and IL-33-dependent mechanisms that underlie severe asthma exacerbations.

133 e is known about the genetic determinants of severe asthma exacerbations.

134 t modules were also significantly reduced in severe asthma except for 3 associated with inflammatory

135 ew genetic studies that focus on moderate-to-severe asthma exist.

136 o tailored treatment for young children with severe asthma exists.

137 Although children with severe asthma experience significant comorbidities and a

138 components most differentiated subjects with severe asthma from other subjects.

139 ken from an unselected subset of adults with severe asthma from the U-BIOPRED cohort.

140 t metrics when differentiating patients with severe asthma from those with nonsevere asthma and healt

141 Patients with severe asthma generally benefit from consultation with a

142 and probabilistic causal methods to identify severe asthma genes and their master regulators.

143 cebo-controlled trial in which patients with severe asthma (GINA 4-5; n = 121) reporting URTI symptom

144 (r = 0.76), with a larger effect size in the severe asthma group.

145 ic data from the U-BIOPRED cohort identified severe asthma groups with features consistent with the p

146 way mucosal CCL26 expression and moderate-to-severe asthma had Feno values (>/=35 ppb) and/or high bE

147 Participants with severe asthma had higher connectivity among components,

148 Children with clinically severe asthma had significantly higher VDP and number of

149 28 with mild-to-moderate asthma and 39 with severe asthma) had a median VDP of 3.75% (1.2% [first qu

150 Since then, the heterogeneity of severe asthma has been explored and the importance of im

151 ype 2 inflammation pathway for patients with severe asthma has resulted in the recognition of an alle

152 New therapeutic options for severe asthma have recently emerged, mostly in the form

153 The majority of patients with mild-to-severe asthma have what is deemed "type-2 high" asthma,

154 rticosteroid responsiveness in subjects with severe asthma heralded the beginning of phenotyping asth

155 17A production has been associated with more severe asthma; however, the mechanisms whereby IL-17A ca

156 ing are features of chronic diseases such as severe asthma, idiopathic pulmonary fibrosis, and system

157 of nonsmokers, this sets the stage for more severe asthma if both mother and grandmother had smoked

158 Cases were defined as having moderate-to-severe asthma if they were taking appropriate medication

159 In patients with severe asthma, imatinib decreased airway hyperresponsive

160 asthma in childhood is often associated with severe asthma in adulthood.

161 ial DNAm were observed between nonsevere and severe asthma in African American children, a subset of

162 ed development of TH17-mediated neutrophilic severe asthma in both acute and chronic HDM-driven model

163 The pathogenesis of severe asthma in childhood remains poorly understood.

164 ttle is known regarding the heterogeneity of severe asthma in children, particularly inflammatory sig

165 rbid allergic diseases are characteristic of severe asthma in children.

166 ledge, this is the first report of a case of severe asthma in which mepolizumab administration revers

167 nchial epithelial samples from patients with severe asthma (in two independent analyses, p=0.039 and

168 cant signals of association with moderate-to-severe asthma, including several signals in innate or ad

169 Severe asthma is a heterogeneous condition, as shown by

170 Effective treatment for severe asthma is a significant unmet need.

171 does not therefore support the concept that severe asthma is associated with corticosteroid resistan

172 Oral corticosteroid (OCS) treatment for severe asthma is associated with substantial disease bur

173 Adult-onset severe asthma is characterized by highly symptomatic dis

174 Adult-onset severe asthma is characterized by inflammatory pathways

175 a may be a separate asthma endotype and that severe asthma is not a single entity, but an extreme end

176 Furthermore, this severe asthma is resistant to steroids and characterized

177 However, the role of allergy in severe asthma is still under debate.

178 usitis, but the role of MUC1 in uncontrolled severe asthma is unknown.

179 /=18 years) as compared with childhood-onset severe asthma (<18 years) were selected from the U-BIOPR

180 icosteroid efficacy is an important issue in severe asthma management and may lead to poor asthma con

181 In parallel, biologics are revolutionizing severe asthma management, mostly in T2 high patients.

182 Data were available for 100 subjects with severe asthma (median age 55 years; 42% males).

183 Severe asthma might be associated with overexpression of

184 Comparisons to severe asthma multicenter studies and available registri

185 comparator cohort of women with moderate-to-severe asthma (n = 1153), termed the Quebec External Com

186 idation testing in independent children with severe asthma (n = 21) and mild/moderate asthma (n = 154

187 BEC) and blood neutrophils from uncontrolled severe asthma (n = 27), controlled mild asthma (n = 16),

188 of children with mild-to-moderate (n = 8) or severe asthma (n = 9), and healthy controls (n = 9).

189 ging Efficacy And Safety With Mepolizumab in Severe Asthma, NCT01000506).

190 racterized cohort, half of the children with severe asthma no longer had severe asthma after 3 years;

191 ng patients with SA, smokers/ex-smokers with severe asthma, nonsmoking patients with mild/moderate as

192 e asthma with fungal sensitization (n = 16), severe asthma not sensitized to fungi (n = 9), mild asth

193 piratory tract, has not been well studied in severe asthma.Objectives: To identify new biomolecular m

194 ed the use of bronchial thermoplasty (BT) in severe asthma.Objectives: We sought to evaluate the effe

195 iations were found between periodontitis and severe asthma, (odds ratio [OR](adjusted]) : 4.00; 95% c

196 ial biopsies of 81 patients with moderate-to-severe asthma of the U-BIOPRED cohort.

197 a suggest that IL-13 may play a dual role in severe asthma: on the one hand driving pathologic cortic

198 re found in association with the presence of severe asthma (OR(adjusted) : 2.64; 95% CI: 1.62 to 4.39

199 of continuous OCS exposure in patients with severe asthma, our results suggest that each OCS prescri

200 ely whether well-characterized children with severe asthma outgrow their asthma during adolescence.

201 s, only 30% of subjects met the criteria for severe asthma (P < .001 compared with enrollment).

202 In some patients with moderate-to-severe asthma, particularly those with noneosinophilic i

203 an adverse role for neutrophils in pediatric severe asthma pathophysiology.

204 clarify underlying non-type-2 mechanisms in severe asthma pathways and possible therapeutic targets.

205 cells and peripheral blood neutrophils from severe asthma patients compared with mild asthma and hea

206 show that mast cell tryptase is elevated in severe asthma patients independent of type 2 biomarker s

207 Severe asthma patients with high blood eosinophils or lo

208 Severe asthma patients with low type 2 inflammation deri

209 atics (including 16 mild, 19 moderate and 22 severe asthma patients) and compared them with 19 health

210 Children with asthma and severe asthma performed slightly better in school than c

211 ne showed lower anti-inflammatory effects in severe asthma peripheral blood neutrophils and HBECs sti

212 play a non-redundant role in patients with a severe asthma phenotype.

213 Our aim was to identify severe asthma phenotypes based on sputum microbiome prof

214 We aimed (1) to identify severe asthma phenotypes using exhaled metabolomic finge

215 are treatments for distinct but overlapping severe asthma phenotypes.

216 and can qualify as noninvasive assessment of severe asthma phenotypes.

217 lugs and airflow obstruction associated with severe asthma phenotypes.

218 osis, chronic obstructive pulmonary disease, severe asthma, pre-existing pulmonary lesions, and sever

219 from healthy control subjects, patients with severe asthma receiving ICSs (n = 174), and patients wit

220 utcomes for this analysis were time to first severe asthma-related event (SARE; hospital admission, e

221 Many patients with severe asthma rely on oral glucocorticoids to manage the

222 Subsets of patients with severe asthma remain symptomatic despite prolonged, high

223 ate and acquired immunity, but their role in severe asthma remains ill-defined.

224 The mechanism underlying nonsevere and severe asthma remains unclear, although it is commonly a

225 derstand the clinical features and to manage severe asthma, representing a non-negligible socioeconom

226 Severe asthma represents a major unmet clinical need; un

227 nal data from participants in phase 3 of the Severe Asthma Research Program (NCT01606826) were used.

228 In the Severe Asthma Research Program (SARP) III cohort, we det

229 Baseline data from the NHLBI Severe Asthma Research Program (SARP)-3 were analyzed.

230 to less than 18 years (107 SA) in the NHLBI Severe Asthma Research Program III were characterized be

231 as performed in participants enrolled in the Severe Asthma Research Program phase 1/2.

232 clusters were validated using an independent Severe Asthma Research Program test set.

233 om 346 adult participants with asthma in the Severe Asthma Research Program with paired (before and 2

234 National Heart, Lung, and Blood Institute's Severe Asthma Research Program, a prospective observatio

235 sputum from 399 patients with asthma in the Severe Asthma Research Program-3 and in 94 healthy contr

236 s and Main Results: We found that 13% of the Severe Asthma Research Program-3 cohort is "eDNA-high,"

237 putum cells from 330 participants in SARP-3 (Severe Asthma Research Program-3) and 79 healthy control

238 tion data were analyzed in 406 adults in the Severe Asthma Research Program-3.

239 tional genes/SNPs for asthma severity in the Severe Asthma Research Program.

240 to which eosinophilic airway inflammation in severe asthma responds to treatment with systemic cortic

241 MUC1 expression in neutrophils from mild and severe asthma (rho = -0.71; P < 0.0001).

242 RATIONALE: Phenotypic distinctions between severe asthma (SA) and nonsevere asthma (NONSA) may be c

243 ression in sputum samples from patients with severe asthma (SA) compared with nonsmoking patients wit

244 RATIONALE: Severe asthma (SA) is a heterogeneous disease with multi

245 A proportion of patients with severe asthma (SA) show poor responses to traditional as

246 atory and clinical outcomes of patients with severe asthma (SA).

247 genetic variants associated with moderate-to-severe asthma, see whether previously identified genetic

248 nt in patients with uncontrolled moderate-to-severe asthma significantly reduced asthma exacerbations

249 Aspirin-exacerbated respiratory disease, a severe asthma subtype, is characterized by exaggerated e

250 ssing CEACAM6 was significantly increased in severe asthma, suggesting the presence of an altered neu

251 The apparent severe asthma symptoms were considered to reflect VCD, a

252 f several new biologics for the treatment of severe asthma-targeting specific endotypes and phenotype

253 d were more frequently used in patients with severe asthma than in those with milder disease.

254 g young children with adrenal dysfunction or severe asthma that are treated with high doses of inhale

255 s study identifies an autoimmune endotype of severe asthma that can be identified by the presence of

256 ing revealed 2 distinct robust phenotypes of severe asthma that exhibited relative overtime stability

257 s been used for the treatment of moderate-to-severe asthma that is not controlled by inhaled steroids

258 ated with the risk of developing moderate-to-severe asthma that regulate mucin production.

259 nts with eosinophils >/=300/muL or with more severe asthma, this rate reduction was significantly mor

260 cterize the role of activated neutrophils in severe asthma through measurement of NETs and inflammaso

261 nd some of the challenges and unmet needs in severe asthma to achieve the goal of delivering individu

262 New biological therapies for treatment of severe asthma, together with developments in biomarkers,

263 d similar experience in a young patient with severe asthma treated with dupilumab.

264 geting these type-2 pathways has transformed severe asthma treatment, but necessitates robust clinica

265 The odds ratio in favor of resolution of severe asthma was 2.75 (95% CI, 1.02-7.43) for those wit

266 with mild/moderate compared with those with severe asthma was in the network of connections between

267 had similar demographic characteristics, but severe asthma was more common in the omalizumab versus t

268 ssion on B, T, and NK cells and monocytes in severe asthma was significantly increased.

269 l brushings of 107 subjects with moderate to severe asthma were annotated by gene set variation analy

270 children aged 5 to 17 years with moderate to severe asthma were enrolled in a 12-month randomized con

271 adult-onset as compared with childhood-onset severe asthma were identified in nasal brushings (5 sign

272 nd environmental exposures and predictive of severe asthma were identified.

273 for guided BT.Methods: Thirty subjects with severe asthma were imaged with volumetric computed tomog

274 Patients with mild/moderate and severe asthma were investigated before and after 2 weeks

275 ate-onset asthma." Children with moderate-to-severe asthma were present in each cluster.

276 patients with poorly controlled, moderate-to-severe asthma were scanned with hyperpolarized (3)He MRI

277 ents with moderate asthma, and patients with severe asthma were stained for OSM and neutrophil elasta

278 atments that target this sub-phenotype(s) of severe asthma, where there is an unmet need.

279 of patients with well-controlled moderate-to-severe asthma, whereas cluster T2 is a group of patients

280 hoid cells were more enriched in adult-onset severe asthma, whereas signatures associated with induce

281 followed up exhaled molecular phenotypes of severe asthma, which were associated with changing infla

282 severe allergic and refractory eosinophilic severe asthma, while in other inflammatory respiratory d

283 of other treatment options for patients with severe asthma who are using regular OCS.

284 reation of subgroups among the patients with severe asthma who differed in molecular responses to ora

285 imatinib in patients with poorly controlled severe asthma who had airway hyperresponsiveness despite

286 n sputum mark a subset of patients with more severe asthma who have NETs and markers of inflammasome

287 acologic intervention to treat patients with severe asthma who present with TH17-mediated neutrophili

288 here a case study of a 13-year-old girl with severe asthma who switched from omalizumab to mepolizuma

289 er T2 is a group of patients with late-onset severe asthma with a history of smoking and chronic airf

290 Bronchopulmonary aspergillosis (n = 16), severe asthma with fungal sensitization (n = 16), severe

291 Indeed, the term severe asthma with fungal sensitization (SAFS) has been

292 allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitization.

293 allergic bronchopulmonary aspergillosis and severe asthma with fungal sensitization.

294 Class 2 represented severe asthma with impaired lung function despite high d

295 Children with severe asthma with inadequate symptom control despite th

296 d of obese female patients with uncontrolled severe asthma with increased exacerbations but with norm

297 ts with a mix of patients with nonsevere and severe asthma with marginal inflammation who exhibited a

298 ed by the use of NPPV in children with acute severe asthma with respiratory muscle fatigue and failur

299 ents, and group 2 participants also had more severe asthma (with regard to asthma control, treatments

300 asty (BT) has been reported in patients with severe asthma, yet its effect on different bronchial str