ライフサイエンスコーパス: airway hyperreactivity

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

2 rway eosinophilia, mucus hypersecretion, and airway hyperreactivity.

3 y, increased mucus production/secretion, and airway hyperreactivity.

4 ation significantly reduces inflammation and airway hyperreactivity.

5 for worm expulsion, tissue inflammation, or airway hyperreactivity.

6 -induced mucus production, inflammation, and airway hyperreactivity.

7 e subsequent development of allergen-induced airway hyperreactivity.

8 lmonary DCs suppressed lung inflammation and airway hyperreactivity.

9 tors, pulmonary eosinophil accumulation, and airway hyperreactivity.

10 ading to allergic pulmonary inflammation and airway hyperreactivity.

11 ergen-induced peribronchial inflammation and airway hyperreactivity.

12 increased pulmonary B and T lymphocytes, and airway hyperreactivity.

13 IL-13), which were associated with increased airway hyperreactivity.

14 o CRA-induced peribronchial inflammation and airway hyperreactivity.

15 sensitization to environmental allergens and airway hyperreactivity.

16 evelopment of peribronchial inflammation and airway hyperreactivity.

17 hyperplasia, increased mucus secretion, and airway hyperreactivity.

18 increases acetylcholine release and leads to airway hyperreactivity.

19 s was found to be negatively correlated with airway hyperreactivity.

20 and acceleration of severe allergen-induced airway hyperreactivity.

21 hich might have a role in the development of airway hyperreactivity.

22 mice with anti-IL-13 substantially inhibited airway hyperreactivity.

23 ll hyperplasia, and significantly attenuated airway hyperreactivity.

24 en, which induced pulmonary eosinophilia and airway hyperreactivity.

25 lenge prevents M(2) receptor dysfunction and airway hyperreactivity.

26 nduction of allergic airway inflammation and airway hyperreactivity.

27 ed, whereas exogenous IL-18 had no effect on airway hyperreactivity.

28 age fluid eosinophils, mucus production, and airway hyperreactivity.

29 of the key physiological endpoint of asthma, airway hyperreactivity.

30 associated with the induction of reversible airway hyperreactivity.

31 of alternatively activated macrophages, and airway hyperreactivity.

32 a role in both the inflammatory response and airway hyperreactivity.

33 eversible airflow obstruction resulting from airway hyperreactivity.

34 ecific subsets of cells and the induction of airway hyperreactivity.

35 ha or RANTES did not affect the intensity of airway hyperreactivity.

36 RANTES or MIP-1alpha, significantly reduced airway hyperreactivity.

37 Th2-cell-induced pulmonary eosinophilia and airway hyperreactivity.

38 features of the allergic response including airway hyperreactivity.

39 population of neurons that are required for airway hyperreactivity.

40 y capacities and efficiently dampen allergic airway hyperreactivity.

41 then challenged with IL-33 and assessed for airway hyperreactivity.

42 rtant role in influenza-induced and allergic airway hyperreactivity.

43 n of growth factors, thereby predisposing to airway hyperreactivity.

44 om dermatitis resulted in increased allergic airway hyperreactivity.

45 aplasia, subepithelial fibrosis and enhanced airway hyperreactivity.

46 uscle in CLE, which related significantly to airway hyperreactivity.

47 lavage concentrations of CXC chemokines, and airway hyperreactivity.

48 nfiltration and prevented the development of airway hyperreactivity.

49 their activities influence functions such as airway hyperreactivity.

50 hypersecretion, Th2 cytokine production, and airways hyperreactivity.

51 iving postnatally, but develop emphysema and airways hyperreactivity.

52 the capacity to induce lung inflammation and airway hyperreactivity, a cardinal asthma feature.

53 onary NKT cells and unexpectedly resulted in airway hyperreactivity, a cardinal feature of asthma, in

54 complications of sickle cell disease include airway hyperreactivity, acute chest syndrome, chronic si

55 tch to persistent mucous cell metaplasia and airway hyperreactivity after clearance of replicating vi

56 to aberrant parasympathetic innervation and airway hyperreactivity after postnatal reinfection.

57 increased inflammation, a high incidence of airway hyperreactivity (AH), and increased circulating l

58 hypothesized that hyaluronan contributes to airway hyperreactivity (AHR) after exposure to ambient o

59 iciency, T-bet(-/-) mice develop spontaneous airway hyperreactivity (AHR) and airway inflammation.

60 nflammatory disorder that is associated with airway hyperreactivity (AHR) and driven by Th2 cytokine

61 ignificantly attenuated airway inflammation, airway hyperreactivity (AHR) and goblet cell hyperplasia

62 a is a respiratory disorder characterized by airway hyperreactivity (AHR) and inflammation and is ass

63 ll tolerance and prevents the development of airway hyperreactivity (AHR) and inflammation, we examin

64 n regulating ILC2 function and ILC2-mediated airway hyperreactivity (AHR) and lung inflammation.

65 T4(-/-) mice showed significant decreases in airway hyperreactivity (AHR) and peribronchial eosinophi

66 ng, shortness of breath, and coughing due to airway hyperreactivity (AHR) and reversible airway obstr

67 cells develop in vivo in a model of chronic airway hyperreactivity (AHR) and what factors control th

68 neutrophilic/ eosinophilic inflammation, and airway hyperreactivity (AHR) at 5 h after dry air challe

69 cription, MOL 294 on airway inflammation and airway hyperreactivity (AHR) in a mouse model of asthma.

70 to play a critical role in the induction of airway hyperreactivity (AHR) in animal models and are as

71 9 strain induced significant dose-responsive airway hyperreactivity (AHR) in BALB/c mice at days 6 an

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

73 f NF-kappaB p65 and p50 subunits, as well as airway hyperreactivity (AHR) in nonallergic mice.

74 hallenge period reduced methacholine-induced airway hyperreactivity (AHR) in OVA- and HDM-sensitized

75 Airway hyperreactivity (AHR) is a key feature of bronchi

76 The impact of airway hyperreactivity (AHR) on respiratory mortality an

77 results in a failure of mice to generate an airway hyperreactivity (AHR) response on both the BALB/c

78 f allergic inflammation that is required for airway hyperreactivity (AHR) to methacholine (MCh).

79 ression ratios, airway obstruction (AO), and airway hyperreactivity (AHR) were significantly increase

80 iNKT cells are required for the induction of airway hyperreactivity (AHR), a cardinal feature of asth

81 ) cells is sufficient for the development of airway hyperreactivity (AHR), a cardinal feature of asth

82 ent mice, we show here that allergen-induced airway hyperreactivity (AHR), a cardinal feature of asth

83 to allergen, can inhibit the development of airway hyperreactivity (AHR), a cardinal feature of asth

84 IL-5 and IL-13, which cause eosinophilia and airway hyperreactivity (AHR), a cardinal feature of asth

85 h resulted in obesity and the development of airway hyperreactivity (AHR), a cardinal feature of asth

86 echanism of nonallergic asthma that leads to airway hyperreactivity (AHR), a cardinal feature of asth

87 ll-independent conditions that might lead to airway hyperreactivity (AHR), a cardinal feature of asth

88 the mice as adults against allergen-induced airway hyperreactivity (AHR), a cardinal feature of asth

89 The development of airway hyperreactivity (AHR), a cardinal feature of asth

90 istic of asthma, including mucus metaplasia, airway hyperreactivity (AHR), and airway inflammation.

91 ls: ozone exposure for air pollution-induced airway hyperreactivity (AHR), and ovalbumin (OVA)-induce

92 have been associated with the development of airway hyperreactivity (AHR), but the specific immunolog

93 er this impairment affected allergen-induced airway hyperreactivity (AHR), CD81(-/-) BALB/c mice and

94 inflammation and by a central feature called airway hyperreactivity (AHR), development of which requi

95 Airway hyperreactivity (AHR), IgE, inflammatory cells, c

96 llergic asthma, including IgE, goblet cells, airway hyperreactivity (AHR), inflammatory cells, cytoki

97 Airway hyperreactivity (AHR), lung inflammation, and ato

98 sed Th2-driven inflammation but also reduced airway hyperreactivity (AHR), mucus hypersecretion, and

99 CD25+ T cells to OVA-sensitized mice reduced airway hyperreactivity (AHR), recruitment of eosinophils

100 hed allergen-induced airway inflammation and airway hyperreactivity (AHR), the cardinal features of a

101 e the cellular immune events contributing to airway hyperreactivity (AHR), we studied an in vivo mous

102 nophilia, it is nevertheless associated with airway hyperreactivity (AHR), which is a cardinal featur

103 oline, to assess airway obstruction (AO) and airway hyperreactivity (AHR).

104 t Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR).

105 le (ASM) innervation (P<0.05) and persistent airway hyperreactivity (AHR).

106 tion, recruitment of inflammatory cells, and airway hyperreactivity (AHR).

107 This disease is characterized by airway hyperreactivity (AHR, defined by exaggerated airf

108 producing cells to investigate their role in airways hyperreactivity (AHR).

109 f allergen challenge significantly increased airway hyperreactivity, airway eosinophil accumulation,

110 of antigen-specific IgG1 and IgE antibodies, airway hyperreactivity, airway inflammation and airway r

111 o chronic pulmonary disease characterized by airway hyperreactivity, airway obstruction, and histolog

112 ineered to express latent TGF-beta abolished airway hyperreactivity and airway inflammation induced b

113 gonucleotides can attenuate the magnitude of airway hyperreactivity and airways remodeling produced i

114 ce and protection against the development of airway hyperreactivity and asthma.

115 This was indicated by decreases in airway hyperreactivity and changes in lung chemokine pro

116 junction but not alone, resulting in reduced airway hyperreactivity and collagen deposition.

117 elopment of allergen- and rhinovirus-induced airway hyperreactivity and decreased eosinophil recruitm

118 not Hutterite homes significantly inhibited airway hyperreactivity and eosinophilia.

119 ound active when tested orally in LPS-evoked airway hyperreactivity and fully confirmed the working h

120 t in both late-phase bronchoconstriction and airway hyperreactivity and furthermore suggest that a ph

121 mice, blockade of IL-13 partially inhibited airway hyperreactivity and goblet cell hyperplasia but n

122 s, but also triggers a chronic response with airway hyperreactivity and goblet cell hyperplasia lasti

123 ice, instillation of MCP-1 induced prolonged airway hyperreactivity and histamine release.

124 atory mucosa can indeed regulate Th2-induced airway hyperreactivity and inflammation and suggest that

125 s in the development of the allergen-induced airway hyperreactivity and inflammation associated with

126 Th1 cells did not attenuate Th2 cell-induced airway hyperreactivity and inflammation in either SCID m

127 el of such reversal was established in which airway hyperreactivity and inflammation in ovalbumin-sen

128 st, OVA-specific Th1 cells failed to inhibit airway hyperreactivity and inflammation in this system.

129 rin-deficient mice had less allergen-induced airway hyperreactivity and inflammation than did control

130 ntratracheally before Ag challenge mitigated airway hyperreactivity and inflammation.

131 ecific Th2 and Th0 cells induced significant airway hyperreactivity and inflammation.

132 Induction of airway hyperreactivity and lung inflammation increased l

133 ged with aerosolized OVA exhibited levels of airway hyperreactivity and lung tissue eosinophil infilt

134 Thus, CD8+ T cells play a role in airway hyperreactivity and M2R dysfunction of sensitized

135 e for a novel innate pathway that results in airway hyperreactivity and may help to explain how TIM-1

136 13Ralpha1 was essential for allergen-induced airway hyperreactivity and mucus hypersecretion but not

137 Again, there was an increase in airway hyperreactivity and mucus production, and goblet

138 mice with imatinib significantly attenuated airway hyperreactivity and peribronchial eosinophil accu

139 ivo, significantly reducing allergen-induced airway hyperreactivity and peribronchial eosinophilic in

140 airway disease is associated with persistent airway hyperreactivity and remodeling, but little is kno

141 c asthma, they were redundant in maintaining airway hyperreactivity and remodeling.

142 phagy pathway, causes unprovoked spontaneous airway hyperreactivity and severe neutrophilic lung infl

143 ng the strong association between asthma and airway hyperreactivity and sickle cell disease, as well

144 lung inflammation resulted in prevention of airway hyperreactivity and significant reduction of eosi

145 tokine genes and controls the development of airway hyperreactivity and T cell production of interleu

146 ce deficient for CCR1, we observed decreased airway hyperreactivity and Th2 cytokine production from

147 nflammation and that this contributes to the airway hyperreactivity and Th2-type inflammation seen in

148 secondhand cigarette smoke (SS) exacerbates airways hyperreactivity and Th2 responses in the lung.

149 peak flow variability (dPFV, an indicator of airway hyperreactivity) and indoor particulate matter (P

150 hips with objective outcomes (lung function, airway hyperreactivity, and atopy), asthma medication, a

151 g inflammation, epithelial cell hyperplasia, airway hyperreactivity, and diminished blood oxygen satu

152 H2 cells promote IgE-mediated sensitization, airway hyperreactivity, and eosinophilia.

153 Because AC and airway hyperreactivity are allergic diseases of mucosal

154 Airway tone and airway hyperreactivity are mediated by the parasympathet

155 t airway inflammation, mucus production, and airway hyperreactivity are the major contributors to the

156 ld-type (WT) mice produced the same level of airway hyperreactivity as transfers from CRA-primed WT i

157 at the time of allergen challenge increased airway hyperreactivity as well as airway eosinophil accu

158 nd demonstrated a dose dependent increase in airway hyperreactivity at 4 hours that was maintained at

159 nsitization phase was sufficient to suppress airway hyperreactivity, bronchiolar inflammatory infiltr

160 nd nasal peanut sensitization prime mice for airway hyperreactivity, but the initial mucosal route of

161 d levels of GM-CSF and TNF-alpha, as well as airway hyperreactivity, cellular inflammation, smooth mu

162 Asthma is characterized by airway hyperreactivity, chronic inflammation, and airway

163 As adults, these mice showed enhanced airway hyperreactivity, chronic pulmonary inflammation,

164 emonstrated significantly lower increases in airway hyperreactivity compared with the littermate cont

165 airway inflammation, and the severity of the airway hyperreactivity correlates with the degree of inf

166 in the OVA-immunized and OVA-challenged OVA airway hyperreactivity-diseased littermates 24 h after i

167 The induction of airway hyperreactivity during allergic responses involve

168 responses in the airway are associated with airway hyperreactivity, eosinophil accumulation in the l

169 diet had markedly decreased allergen-induced airway hyperreactivity, eosinophil infiltration, and pro

170 ity with AAL(S) abolished rhinovirus-induced airway hyperreactivity, eosinophil influx, and CCL11, CC

171 rance of conidia and significantly increased airway hyperreactivity, eosinophilia, and peribronchial

172 n the lung exhibited significantly increased airway hyperreactivity, eosinophilia, IL-4 levels, and C

173 s of experimental allergic asthma, including airway hyperreactivity, eosinophilic airway inflammation

174 Allergic conjunctivitis (AC) and airway hyperreactivity exacerbate corneal allograft reje

175 er service in Southwest Asia should focus on airway hyperreactivity from exposures to higher levels o

176 to the same Ag, blockade of IL-13 inhibited airway hyperreactivity, goblet cell hyperplasia, and air

177 control group of mice exhibited significant airway hyperreactivity, goblet cell hyperplasia, and per

178 nfiltrate, eosinophilia, serum anti-OVA IgE, airway hyperreactivity, goblet cell hyperplasia, and pho

179 Herein we describe a model of persistent airway hyperreactivity, goblet cell hyperplasia, and sub

180 ed allergen-specific IgE, lung inflammation, airway hyperreactivity, goblet cell metaplasia, Th2/Th17

181 Pre-exposure to ozone resulted in enhanced airway hyperreactivity, higher concentrations of both to

182 M33-null mice showed normal allergen-induced airway hyperreactivity, immunoglobulin E production, muc

183 cockroach allergen-induced inflammation and airway hyperreactivity in a mouse model of asthma.

184 line receptor M3 prevents the progression of airway hyperreactivity in a mouse model of childhood ast

185 een demonstrated to prevent inflammation and airway hyperreactivity in a murine model of asthma.

186 caused peribronchial fibrosis, resulting in airway hyperreactivity in adult mice.

187 erably attenuated pulmonary inflammation and airway hyperreactivity in BALB/c recipient mice in respo

188 ponses in the lung have been associated with airway hyperreactivity in both human asthma and in murin

189 pment of mucous cell metaplasia and possibly airway hyperreactivity in experimental models and in hum

190 Because glucocorticoids inhibit airway hyperreactivity in humans and in animal models of

191 inhibit allergic pulmonary inflammation and airway hyperreactivity in murine models of asthma.

192 n-1 (MCP-1), a CC (beta) chemokine, mediates airway hyperreactivity in normal and allergic mice.

193 since it contributes to mucus production and airway hyperreactivity in our model of RSV infection.

194 A murine model of airway hyperreactivity in response to acetylcholine was

195 by either i.n. or i.p. routes did not reduce airway hyperreactivity in response to methacholine chall

196 phil infiltration, mucus hypersecretion, and airway hyperreactivity in response to methacholine chall

197 The examination of RSV-induced airway hyperreactivity in STAT6(-/-) mice demonstrated a

198 he indications of the diagnosis of bronchial airway hyperreactivity in subjects who do not have clini

199 ction, airway smooth muscle alterations, and airways hyperreactivity in a memory CD4(+) T cell-depend

200 Having airway hyperreactivity increased the risk of rapid decli

201 Previous studies using OVA-induced airway hyperreactivity indicated that P-selectin, a memb

202 Asthma has multiple features, including airway hyperreactivity, inflammation and remodelling.

203 irway disease is characterized by persistent airway hyperreactivity, inflammation, and fibrosis.

204 Subsequent tissue damage leading to airway hyperreactivity is a result of activation of mult

205 In antigen-challenged guinea pigs, airway hyperreactivity is due to recruitment of eosinoph

206 Thus, in these mice, basal airway hyperreactivity is maintained independently of ty

207 the conidia burden but significantly reduced airway hyperreactivity, lung IL-4 levels, and lymphocyte

208 Airway hyperreactivity, measured by the methacholine-pro

209 e with anti-IL-12 resulted in an increase in airway hyperreactivity, mucus production, and airway inf

210 like ligand (Dll)-4, significantly decreased airway hyperreactivity, mucus production, and Th2 cytoki

211 nodes and lung, and prevented eosinophilia, airway hyperreactivity, mucus secretion, and Th2 cyto-ki

212 th channelrhodopsin dramatically exacerbates airway hyperreactivity of inflamed airways.

213 ally and nasally sensitized mice experienced airway hyperreactivity on nasal peanut challenge.

214 irway inflammation, and, importantly, marked airway hyperreactivity only when allergen exposure occur

215 in resolution of airway inflammation but not airway hyperreactivity or remodeling.

216 cells in the development of allergen-induced airway hyperreactivity, our results strongly suggest tha

217 rgic mice with AMD3100 significantly reduced airway hyperreactivity, peribronchial eosinophilia, and

218 enes (E(-)/P(-)) showed 70-85% reductions in airway hyperreactivity, peribronchial inflammation, and

219 Our results show that the airway hyperreactivity phenotype can be physiologically

220 Airway hyperreactivity, recruitment of infiltrating cell

221 eutralization of CXCR2 resulted in decreased airway hyperreactivity relative to the RSV-infected cont

222 ate IL-4/IL-13 for allergic inflammation and airway hyperreactivity remains unclear.

223 unctional activities including regulation of airway hyperreactivity, resistance to nematode parasites

224 , the remodeling changes did not resolve and airway hyperreactivity resolved only partly.

225 L-13 in inducing and maintaining a prolonged airway hyperreactivity response was examined using a mou

226 The airway hyperreactivity response was significantly increa

227 Thus, we propose that later airway hyperreactivity results from selective retention

228 such that allergen sensitization and severe airway hyperreactivity subsequently occurred.

229 nce generated from a mouse model of allergic airway hyperreactivity suggests that disordered coagulat

230 Conversely, airway hyperreactivity, suppressed as a result of long-t

231 c ovalbumin-induced allergic airway disease, airway hyperreactivity, T(H)2 responses, mucus hypersecr

232 d significantly greater methacholine-induced airway hyperreactivity than did CXCR2+/+ mice.

233 aling plays a more important in vivo role in airways hyperreactivity than IL-25.

234 Airway hyperreactivity that follows exposure to antigen

235 e substantial abrogation of allergen-induced airway hyperreactivity, these gene deletions had no impa

236 roxia exposure causes detrimental effects on airway hyperreactivity through microRNA-342-3p-mediated

237 ocytes in the peribronchial area, and severe airway hyperreactivity through whole-body plethysmograph

238 Human asthma is characterized by increased airway hyperreactivity to a variety of bronchoconstricti

239 Sephadex instillation also induced airway hyperreactivity to acetylcholine and bradykinin.

240 ippostrongylus brasiliensis, or induction of airway hyperreactivity to aerosolized antigen, beta 2m-d

241 production, and almost completely abolished airway hyperreactivity to contractile stimuli.

242 (40%) patients demonstrated some evidence of airway hyperreactivity to include eight who met asthma c

243 Similarly, compared with wild-type animals, airway hyperreactivity to inhaled methacholine (40 micro

244 ytes into bronchoalveolar lavage and induced airway hyperreactivity to inhaled methacholine.

245 lavage eosinophilia, lung eosinophilia, and airway hyperreactivity to methacholine in a mouse model

246 Airway hyperreactivity to methacholine observed on Day 7

247 as well as increased collagen deposition and airway hyperreactivity to methacholine were all clearly

248 nflammation, airway remodeling, or increased airway hyperreactivity to methacholine.

249 dition, HDM-exposed mice demonstrated severe airway hyperreactivity to methacholine.

250 ipid mediators, and more rapid resolution of airway hyperreactivity to methacholine.

251 Depletion of MCP-1 significantly reduced the airway hyperreactivity to near control levels, whereas d

252 posure can attenuate inflammation and revert airway hyperreactivity to normal responsiveness.

253 mmation, reversible bronchoconstriction, and airway hyperreactivity to provocative stimuli.

254 Reversible airway hyperreactivity underlies the pathophysiology of

255 rotrophic pathways predisposing to postnatal airway hyperreactivity upon reinfection with the virus.

256 pared to that in MpP mice (P = 0.048), while airway hyperreactivity was also elevated in MpIL12 mice

257 Airway hyperreactivity was mediated by MCP-1 through CCR

258 Interestingly, airway hyperreactivity was significantly decreased at ea

259 To examine the direct role of SCF on airway hyperreactivity, we administered SCF into the air

260 ired for the development of allergen-induced airway hyperreactivity, we hypothesized that natural kil

261 VA-Th1 cells during experimental OVA-induced airway hyperreactivity, we injected 10(7 64)Cu-OVA-Th1 c

262 as direct MCP-1 instilled-induced changes in airway hyperreactivity were significantly attenuated in

263 ubepithelial fibrosis, mucus metaplasia, and airway-hyperreactivity were also attenuated by VE-cadher

264 muscle layer, increased mucus, and increased airway hyperreactivity which was significantly enhanced

265 parental tobacco smoking was associated with airway hyperreactivity, which could contribute to lower

266 In vivo, asperamide B rapidly induced airway hyperreactivity, which is a cardinal feature of a

267 each airway challenge significantly reduced airway hyperreactivity, with a concomitant decrease in e