ライフサイエンスコーパス: airway hyperresponsiveness

1 lung inflammation, cellular infiltrate, and airway hyperresponsiveness.

2 s in increased aeroantigen sensitization and airway hyperresponsiveness.

3 uppressed IL-1beta-induced steroid-resistant airway hyperresponsiveness.

4 cytokine levels, goblet cell metaplasia, and airway hyperresponsiveness.

5 ion, potentially promoting sensitization and airway hyperresponsiveness.

6 roid-resistant neutrophilic inflammation and airway hyperresponsiveness.

7 d by inflammation, mucus hypersecretion, and airway hyperresponsiveness.

8 ety and useful in the diagnosis of bronchial airway hyperresponsiveness.

9 odies, in parasympathetic-mediated asthmatic airway hyperresponsiveness.

10 ion, which leads to mucus hypersecretion and airway hyperresponsiveness.

11 uced airway mucus production, and attenuated airway hyperresponsiveness.

12 ed mucus production together with pronounced airway hyperresponsiveness.

13 ormal lung function, and a greater degree of airway hyperresponsiveness.

14 ilic esophageal infiltration, and suppressed airway hyperresponsiveness.

15 n in airway inflammation, IgE Ab levels, and airway hyperresponsiveness.

16 ict allergen-induced airway inflammation and airway hyperresponsiveness.

17 (EIB) is a prototypical feature of indirect airway hyperresponsiveness.

18 ergic sensitization, airway inflammation and airway hyperresponsiveness.

19 haled air, blood and sputum eosinophils, and airway hyperresponsiveness.

20 zation prevented DEP-induced exacerbation of airway hyperresponsiveness.

21 by 82-96% (p </= 0.001) and fully normalized airway hyperresponsiveness.

22 acterized by chronic airway inflammation and airway hyperresponsiveness.

23 c pulmonary inflammation, and development of airway hyperresponsiveness.

24 associated with behavioral inhibition and/or airway hyperresponsiveness.

25 the therapeutic benefit of MSC treatment on airway hyperresponsiveness.

26 d cellular infiltration in BALF and allergic airway hyperresponsiveness.

27 and neutrophilic inflammation, but very mild airway hyperresponsiveness.

28 c effects on systemic allergic responses and airway hyperresponsiveness.

29 -13/GM-CSF) and a partial protection against airway hyperresponsiveness.

30 ted, IL-13 increased airway inflammation and airway hyperresponsiveness.

31 ssion, ILC2 expansion, mucus metaplasia, and airway hyperresponsiveness.

32 reased neutrophils and IL-17, but equivalent airway hyperresponsiveness.

33 These changes were independent from airway hyperresponsiveness.

34 ogical processes leading to inflammation and airway hyperresponsiveness.

35 pe 2 cytokine production, IgE secretion, and airway hyperresponsiveness.

36 ILC2s; and exaggerated mucus metaplasia and airway hyperresponsiveness.

37 ding neutrophilic pulmonary inflammation and airway hyperresponsiveness.

38 by diminished eosinophilic inflammation and airway hyperresponsiveness.

39 eosinophilia without affecting IgE levels or airway hyperresponsiveness.

40 abrogation of neutrophilic inflammation and airway hyperresponsiveness.

41 airway epithelial injury, inflammation, and airway hyperresponsiveness.

42 iratory distress in response to allergen and airway hyperresponsiveness.

43 rophin associated with airway remodeling and airway hyperresponsiveness.

44 utically targeted to mitigate the effects of airway hyperresponsiveness.

45 pes enhanced development of allergen-induced airway hyperresponsiveness.

46 hyperactivity, increased ASM contraction and airway hyperresponsiveness.

47 c, and fibrotic mediators and contributes to airways hyperresponsiveness.

48 ophilic inflammation, mucous metaplasia, and airways hyperresponsiveness.

49 cells, mucus production, and development of airways hyperresponsiveness.

50 hich causes persistent mucous metaplasia and airways hyperresponsiveness.

51 thmatic patient-related outcome measures and airways hyperresponsiveness.

52 sistent observation has been the increase in airway hyperresponsiveness, a characteristic of asthma,

53 inistered in murine asthma models attenuated airway hyperresponsiveness, a hallmark of asthma.

54 the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiological marker of se

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

56 Airway hyperresponsiveness (AHR) affects 55%-77% of chil

57 nd allergen coexposure resulted in increased airway hyperresponsiveness (AHR) and accumulation of pat

58 Systemic application of ApoA-IV prevented airway hyperresponsiveness (AHR) and airway eosinophilia

59 ions of S1P and SphK1 to mast cell-dependent airway hyperresponsiveness (AHR) and airway inflammation

60 Airway hyperresponsiveness (AHR) and bronchial inflammat

61 enged mice induced Treg cells and attenuated airway hyperresponsiveness (AHR) and inflammation compar

62 nd on development of ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and inflammation in an

63 role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in mic

64 ntly demonstrated that IVIg protects against airway hyperresponsiveness (AHR) and inflammation in mou

65 Airway hyperresponsiveness (AHR) and inflammation were a

66 tective role of H2S against allergen-induced airway hyperresponsiveness (AHR) and inflammation.

67 basal airway function, bacterial LPS-induced airway hyperresponsiveness (AHR) and lung inflammation,

68 B/c mice resulted in significantly increased airway hyperresponsiveness (AHR) and macrophage and neut

69 We determined airway hyperresponsiveness (AHR) and pulmonary inflammat

70 e during the 4-wk allergen challenge blunted airway hyperresponsiveness (AHR) and reduced fibronectin

71 e (ASM) contractility and the development of airway hyperresponsiveness (AHR) are cardinal features o

72 ance and also increased methacholine-induced airway hyperresponsiveness (AHR) as measured by lung res

73 ls' (aSMCs) contraction and proliferation in airway hyperresponsiveness (AHR) associated with asthma

74 rway smooth muscle (ASM) plays a key role in airway hyperresponsiveness (AHR) but it is unclear wheth

75 Tgfbm3(C57) synergize to reverse accentuated airway hyperresponsiveness (AHR) caused by low TGFbeta1

76 cell (ILC) and TH2 cell numbers but similar airway hyperresponsiveness (AHR) compared with those aft

77 g surfactant protein A (SP-A) have increased airway hyperresponsiveness (AHR) during M pneumoniae inf

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

79 ole of the Nlrp3 inflammasome in nonallergic airway hyperresponsiveness (AHR) has not previously been

80 the development of allergic inflammation and airway hyperresponsiveness (AHR) in acute murine models.

81 vity of cholinergic neurons are mediators of airway hyperresponsiveness (AHR) in asthma, however, mec

82 tors correlates with airway neutrophilia and airway hyperresponsiveness (AHR) in COPD patients.

83 exposure results in greater inflammation and airway hyperresponsiveness (AHR) in obese versus lean mi

84 development of eosinophilic inflammation and airway hyperresponsiveness (AHR) in sensitized individua

85 Although airway hyperresponsiveness (AHR) is a defining feature o

86 Indirect airway hyperresponsiveness (AHR) is a fundamental featur

87 sponses to inhaled allergens, which leads to airway hyperresponsiveness (AHR) to contractile stimuli

88 Airway inflammation, airway hyperresponsiveness (AHR) to inhaled methacholine

89 at high fat diet (HFD) for 2 weeks increases airway hyperresponsiveness (AHR) to methacholine challen

90 VA-asthmatic mice, significant diminution of airway hyperresponsiveness (AHR) was first apparent, whe

91 taining objective evidence of athlete asthma/airway hyperresponsiveness (AHR) were collected for all

92 inflammation, mRNA levels in the lungs, and airway hyperresponsiveness (AHR) were examined.

93 this mechanism may result in a reduction of airway hyperresponsiveness (AHR) when using triple thera

94 te that IL-21R-deficiency reduces HDM-driven airway hyperresponsiveness (AHR) with only partial effec

95 e subjected to this SA model failed to mount airway hyperresponsiveness (AHR) without appreciable eff

96 h2 asthma phenotype that is characterized by airway hyperresponsiveness (AHR) without eosinophilic in

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

98 Asthma is a chronic disease associated with airway hyperresponsiveness (AHR), airway obstruction and

99 ritical for preservation of allergen-induced airway hyperresponsiveness (AHR), airway resistance, and

100 enotypic manifestation of asthma is indirect airway hyperresponsiveness (AHR), and a prominent molecu

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

102 evaluate inflammation, NF-kappaB activation, airway hyperresponsiveness (AHR), and airway remodeling.

103 ere exposed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and mitochondrial func

104 m cells (MSCs) decrease airway eosinophilia, airway hyperresponsiveness (AHR), and remodelling in mur

105 pendent domains labelled from A to E, namely airway hyperresponsiveness (AHR), bronchitis, cough refl

106 y-eight hours after the final OVA challenge, airway hyperresponsiveness (AHR), bronchoalveolar fluid

107 Major features of allergic asthma include airway hyperresponsiveness (AHR), eosinophilic inflammat

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

109 one, additional treatment with sGARP reduced airway hyperresponsiveness (AHR), influx of neutrophils

110 ed the role of IL-13 and IL-17A in mediating airway hyperresponsiveness (AHR), lung inflammation, and

111 allenged wild type mice displayed a striking airway hyperresponsiveness (AHR), mMCP-6(-/-) mice had l

112 In contrast to the anticipated reduction in airway hyperresponsiveness (AHR), OVA allergen-challenge

113 llergic asthma, it is not a prerequisite for airway hyperresponsiveness (AHR), suggesting that underl

114 lates allergic airway inflammation (AAI) and airway hyperresponsiveness (AHR), we compared AAI and AH

115 models of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investiga

116 tissue homeostasis and in obesity-associated airway hyperresponsiveness (AHR).

117 , which has been linked to steroid-resistant airway hyperresponsiveness (AHR).

118 acterized by chronic airway inflammation and airway hyperresponsiveness (AHR).

119 ytokine production, airway inflammation, and airway hyperresponsiveness (AHR).

120 in allergic sensitization, inflammation, and airway hyperresponsiveness (AHR).

121 evidence suggests that IL-17 contributes to airway hyperresponsiveness (AHR); however, the mechanism

122 eling [TGF-beta1, 5-lipoxygenase (5-LO)] and airway-hyperresponsiveness (AHR) (5-LO).

123 We assessed airways hyperresponsiveness (AHR) and lung inflammation

124 hronic inflammatory disease characterized by airways hyperresponsiveness (AHR), reversible airflow ob

125 ant to cigarette smoke-induced inflammation, airway hyperresponsiveness, airspace enlargements, and l

126 enotype was determined by the measurement of airway hyperresponsiveness, airway inflammation, and cyt

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

128 immune response in the lung with features of airway hyperresponsiveness and Ag-specific type 2 airway

129 nflammasome inhibition using CRID3 prevented airway hyperresponsiveness and airway inflammation (both

130 IL-33 enhanced airway hyperresponsiveness and airway inflammation by su

131 IT ameliorated airway hyperresponsiveness and airway inflammation in a

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

133 dels provide evidence that processes evoking airway hyperresponsiveness and airway smooth muscle thic

134 PGE(2) generation in the lung predisposes to airway hyperresponsiveness and aspirin intolerance in as

135 not CD4+ICOS-, cells inhibited BPEx-induced airway hyperresponsiveness and bronchoalveolar lavage eo

136 Conversely, airway hyperresponsiveness and contractile tissue underw

137 mice had an increased propensity to develop airway hyperresponsiveness and displayed significantly e

138 2-lymphocyte driven disease characterized by airway hyperresponsiveness and eosinophilia.

139 33 knockout mice, the IL-33- and OVA-induced airway hyperresponsiveness and eosinophilic airway infla

140 wild-type mice, IL-33 or OVA induced similar airway hyperresponsiveness and eosinophilic airway infla

141 In ST2 knockout mice, IL-33 and OVA induced airway hyperresponsiveness and eosinophilic airway infla

142 asthma with reduced airway mucus production, airway hyperresponsiveness and eosinophils.

143 lung, and bronchoalveolar lavage as well as airway hyperresponsiveness and goblet cell metaplasia we

144 f rest, a single exposure to HDM resulted in airway hyperresponsiveness and increased TH2 cytokine le

145 Exposure to respiratory allergens triggers airway hyperresponsiveness and inflammation characterize

146 Anti-ST2 reduced ozone-induced airway hyperresponsiveness and inflammation in obese mic

147 elivery of anti-IFN-gamma antibodies induced airway hyperresponsiveness and inflammation in wild-type

148 Hypoxia enhances CD8(+) T(C)2 cell-dependent airway hyperresponsiveness and inflammation through HIF-

149 s, HSP65-induced effects on allergen-induced airway hyperresponsiveness and inflammation were associa

150 s, is pivotal in the development of allergic airway hyperresponsiveness and inflammation, and yet rem

151 diated wild-type (WT) recipients exacerbates airway hyperresponsiveness and inflammation, whereas tra

152 d CD8-deficient recipients failed to restore airway hyperresponsiveness and inflammation.

153 In vivo, HSP65 prevented the development of airway hyperresponsiveness and inflammation.

154 irways in vivo, such as bronchoconstriction, airway hyperresponsiveness and inflammatory cell influx

155 may potently induce bronchial constriction, airway hyperresponsiveness and inflammatory cell influx

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

157 Both therapeutic approaches reduced airway hyperresponsiveness and leukocyte infiltration in

158 of Tet1 increased disease severity including airway hyperresponsiveness and lung eosinophilia.

159 or for PARP activity reduced the severity of airway hyperresponsiveness and lung inflammation.

160 iated with it in a model of AAD dependent on airway hyperresponsiveness and lung inflammation.

161 -/-) mice were resistant to the induction of airway hyperresponsiveness and manifested improved lung

162 ed in ROCK2(+/-) vs. wild-type mice, as were airway hyperresponsiveness and mucous hypersecretion.

163 placebo on either methacholine or histamine airway hyperresponsiveness and no change in ACQ or AQLQ.

164 orted that NQO1-null mice are protected from airway hyperresponsiveness and pulmonary inflammation fo

165 This led to suppression of airway hyperresponsiveness and restored steroid sensitiv

166 Airway hyperresponsiveness and serum IgE levels were com

167 terferon levels were associated with greater airway hyperresponsiveness and skin prick test response

168 tion prevented the subsequent enhancement of airway hyperresponsiveness and the development of airway

169 In mice, periostin is required for maximal airways hyperresponsiveness and inflammation after HDM s

170 d near airways and induced mucus metaplasia, airway hyperresponsiveness, and airway eosinophil activa

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

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

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

174 d from allergen-induced tissue inflammation, airway hyperresponsiveness, and goblet cell metaplasia i

175 ted with airway eosinophilia, development of airway hyperresponsiveness, and goblet cell metaplasia,

176 uction, which promoted chronic inflammation, airway hyperresponsiveness, and mucus production during

177 ic phenotype, including airway inflammation, airway hyperresponsiveness, and mucus production.

178 ess atopic sensitization, a lesser degree of airway hyperresponsiveness, and no concomitant allergic

179 monary inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific IgE compare

180 d airway eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OVA-specific IgE product

181 bition reduced allergic airway inflammation, airway hyperresponsiveness, and pulmonary collagen depos

182 o greater viral load, worse airway symptoms, airway hyperresponsiveness, and reductions in lung funct

183 ry cells were related to greater viral load, airway hyperresponsiveness, and reductions in lung funct

184 infection with respiratory syncytial virus, airway hyperresponsiveness, and severe bronchopulmonary

185 ly related to both behavioral inhibition and airway hyperresponsiveness, and so could not mediate the

186 nto the lung, IgE production, development of airway hyperresponsiveness, and Th2 T cell priming.

187 terized by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated inflammatio

188 helium is a critical determinant of indirect airway hyperresponsiveness, and the airway epithelium mi

189 The mechanisms by which airway inflammation, airway hyperresponsiveness, and variable airflow obstruc

190 lationship between behavioral inhibition and airway hyperresponsiveness, and whether hormonal and imm

191 ilia as an indicator of airway infection and airway hyperresponsiveness as an indicator of smooth mus

192 Behaviorally inhibited monkeys had airway hyperresponsiveness as indicated by the methachol

193 Airway hyperresponsiveness, as well as inflammation, and

194 ug significantly attenuated allergen-induced airway hyperresponsiveness at 24 hours after allergen ch

195 s for FEV1, smaller bronchodilator response, airway hyperresponsiveness at baseline, and male sex wer

196 opathologic condition, mucus production, and airway hyperresponsiveness between wild-type and Nlrp3(-

197 rization with H. pylori extract prevents the airway hyperresponsiveness, bronchoalveolar eosinophilia

198 IL-33 induces airway hyperresponsiveness, but its role in airway remod

199 ition in rhesus monkeys (Macaca mulatta) and airway hyperresponsiveness, but not atopy, and the sugge

200 Be2 cells were essential in airway hyperresponsiveness, but not in other parameters.

201 ion and suppression of lung inflammation and airway hyperresponsiveness, but SCIT was associated with

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

203 We measured airway hyperresponsiveness by using flexiVent; inflammat

204 DEP and HDM coexposure markedly enhanced airway hyperresponsiveness compared with HDM exposure al

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

206 Serum allergen-specific antibody levels, airway hyperresponsiveness, cytokine levels in spleen ce

207 Development of airway hyperresponsiveness, cytokine levels, and airway

208 FAO significantly decreased allergen-induced airway hyperresponsiveness, decreased the number of infl

209 with poorly controlled severe asthma who had airway hyperresponsiveness despite receiving maximal med

210 lphavbeta6-deficient mice are protected from airway hyperresponsiveness, due in part to increased exp

211 Live C cladosporioides induced robust airway hyperresponsiveness, eosinophilia, and a predomin

212 med at various time points for evaluation of airway hyperresponsiveness, eosinophilia, mucus producti

213 bited hallmark features of asthma, including airway hyperresponsiveness, eosinophilic accumulation, a

214 3A suppresses Th2 pulmonary inflammation and airway hyperresponsiveness following aeroallergen exposu

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

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

217 yc (iPSC-w/o-c-Myc) in allergic diseases and airway hyperresponsiveness has not been investigated.

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

219 ed tissue ATP levels explain protection from airway hyperresponsiveness, i.e., absence of COX4i2 lead

220 Targeting Axl also inhibited airway hyperresponsiveness, IL-4 and IL-13 production, a

221 Ab production, type 2 cytokine response, and airway hyperresponsiveness in 4 wk, followed by airway r

222 o the blood, lungs, and airways and prevents airway hyperresponsiveness in a mouse eosinophilic asthm

223 h CBFbeta inhibitors prevented ILC2-mediated airway hyperresponsiveness in a mouse model of acute Alt

224 lic lung inflammation, mucus production, and airway hyperresponsiveness in an experimental model of O

225 geted as a new strategy for the treatment of airway hyperresponsiveness in asthma.

226 tin dynamics, smooth muscle contraction, and airway hyperresponsiveness in asthma.

227 nol markedly suppressed methacholine-induced airway hyperresponsiveness in experimental asthma.

228 GF factor 8 (Mfge8(-/-)) develop exaggerated airway hyperresponsiveness in experimental models of ast

229 f type 2 cytokines, airway eosinophilia, and airway hyperresponsiveness in juvenile Scnn1b-Tg mice.

230 Both BAY 41-2272 and BAY 60-2770 reversed airway hyperresponsiveness in mice with allergic asthma

231 kine levels in bronchial fluid, and improved airway hyperresponsiveness in mice.

232 rsed IgE and TH2 cytokine production but not airway hyperresponsiveness in OVA-challenged DNA-PKcs(+/

233 Airway hyperresponsiveness in response to methacholine w

234 and inhibition of GSNO reductase attenuated airway hyperresponsiveness in vivo among juvenile and ad

235 tokine response, mucus cell hyperplasia, and airway hyperresponsiveness in vivo.

236 onary inflammation and the asthma surrogate, airway hyperresponsiveness, in a murine acute model of a

237 RNA-treated mice produced significantly less airway hyperresponsiveness induced by methacholine.

238 Profoundly enhanced airway hyperresponsiveness, inflammation, and fibrosis w

239 An anti-TSLP antibody abrogated airway hyperresponsiveness, inflammation, and mucus prod

240 bination for 8 consecutive days, after which airway hyperresponsiveness, inflammatory cell influx int

241 sPLA(2)-X gene (Pla2g10) display attenuated airway hyperresponsiveness, innate and adaptive immune r

242 Airway hyperresponsiveness is common to atopic and non-a

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

244 ferences were noted between the 2 sexes with airway hyperresponsiveness (mannitol provocation testing

245 ients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell counts, and trypta

246 The primary end point was the change in airway hyperresponsiveness, measured as the concentratio

247 flow limitation, bronchial reversibility, or airway hyperresponsiveness (misdiagnosed asthma).

248 The IL-25-high subset had greater airway hyperresponsiveness, more airway and blood eosino

249 of inhaled corticosteroids, had more severe airway hyperresponsiveness, more often nasal polyps, and

250 roxia induced asthma-like features including airway hyperresponsiveness, mucus hyperplasia, airway eo

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

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

253 gether, PTX3 deficiency results in augmented airway hyperresponsiveness, mucus production, and IL-17A

254 lvement in long-term airway inflammation and airway hyperresponsiveness occurred at least partially v

255 mation (p < 0.001 for all) but did not alter airway hyperresponsiveness or airway remodeling.

256 nset of TH2 immune responses and OVA-induced airway hyperresponsiveness or goblet cell hyperplasia, i

257 tic recipients by </= 23% but did not affect airway hyperresponsiveness or IgE levels, whereas equal

258 mmation (p = 0.045) and increased peripheral airway hyperresponsiveness (p = 0.02), nicotine-free Ban

259 We conclude that obesity leads to the airway hyperresponsiveness preventable by caloric restri

260 with only OVA Ag were sufficient to trigger airway hyperresponsiveness, prominent eosinophilic infla

261 genes (FAM129A, SYNPO2) were associated with airway hyperresponsiveness (provocative concentration of

262 methasone (DEX) in counteracting OVA-induced airway hyperresponsiveness, recruitment of eosinophils,

263 ing and deep inspirations (DI) in modulating airway hyperresponsiveness remains poorly understood.

264 individual involvement in the development of airway hyperresponsiveness remains unexplored.

265 g: SK-1211) in order to get approved for the airway hyperresponsiveness test in Japan.

266 The airway hyperresponsiveness test with SK-1211 was conduct

267 The airway hyperresponsiveness test with SK-1211 was no spec

268 ot mature mice, causes mucous metaplasia and airway hyperresponsiveness that are associated with the

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

270 Airway hyperresponsiveness to aerosolized methacholine w

271 distress in response to allergen and reduces airway hyperresponsiveness to bradykinin.

272 humoral and cellular immunological profiles, airway hyperresponsiveness to bronchospastic stimuli, an

273 ) mice that were exposed to Cl2 demonstrated airway hyperresponsiveness to inhaled methacholine signi

274 mice, and lung allergic responses, including airway hyperresponsiveness to inhaled methacholine, were

275 Induced sputum was obtained, and airway hyperresponsiveness to mannitol and fraction of e

276 The GSTP1 genotype had no effect on airway hyperresponsiveness to methacholine and the react

277 icant deficits in lung function and enhanced airway hyperresponsiveness to methacholine as compared w

278 deficits in their lung function and enhanced airway hyperresponsiveness to methacholine challenge fro

279 evels of fractional exhaled nitric oxide and airway hyperresponsiveness to methacholine were not affe

280 g the past 5 years, which could be: positive airway hyperresponsiveness to methacholine, positive rev

281 tenuated HDM-induced airway inflammation and airway hyperresponsiveness to methacholine.

282 , spontaneous eosinophilic inflammation, and airway hyperresponsiveness to methacholine.

283 l counts in BAL and significantly attenuated airway hyperresponsiveness to methacholine.

284 14 allergen-sensitized participants (9 with airway hyperresponsiveness) underwent inhaled allergen c

285 ) DCs, leading to increased inflammation and airway hyperresponsiveness upon RV infection.

286 Airway hyperresponsiveness was also associated with lowe

287 Improved airway hyperresponsiveness was also observed in mice tha

288 levels were higher in CysLTr1(-/-) mice and airway hyperresponsiveness was ameliorated using a granu

289 ce were challenged with aerosols to HDM, and airway hyperresponsiveness was evaluated by using plethy

290 response in OVA-challenged WT mice, although airway hyperresponsiveness was greater in Stard7(+/-) re

291 Airway hyperresponsiveness was increased in allergen-tre

292 d did not reduce remodeling or IL-33 levels; airway hyperresponsiveness was only partially reduced.

293 portantly, chronic allergic inflammation and airway hyperresponsiveness were dependent on IL-4Ralpha-

294 ILC2 responses, airway inflammation and airway hyperresponsiveness were examined in Balb/c mice

295 ion to wild-type levels, whereas eotaxin and airway hyperresponsiveness were not affected.

296 t cell hyperplasia, collagen deposition, and airway hyperresponsiveness were significantly diminished

297 d immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the

298 Finally, asthma is characterized by airway hyperresponsiveness, which largely stems from air

299 periods to assess incremental improvement in airway hyperresponsiveness while reducing the likelihood

300 acerbated asthma phenotype (inflammation and airway hyperresponsiveness), with increased development