ライフサイエンスコーパス: airway hyperreactivity

1 2 cytokine production, serum IgE levels, and airway hyperreactivity.

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

3 lavage concentrations of CXC chemokines, and airway hyperreactivity.

4 nfiltration and prevented the development of airway hyperreactivity.

5 their activities influence functions such as airway hyperreactivity.

6 rway eosinophilia, mucus hypersecretion, and airway hyperreactivity.

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

8 ation significantly reduces inflammation and airway hyperreactivity.

9 onding eosinophil infiltration and increased airway hyperreactivity.

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

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

12 e subsequent development of allergen-induced airway hyperreactivity.

13 s, lung histology, lung cytokine levels, and airway hyperreactivity.

14 lmonary DCs suppressed lung inflammation and airway hyperreactivity.

15 tors, pulmonary eosinophil accumulation, and airway hyperreactivity.

16 onary type 2 cytokine responses and allergic airway hyperreactivity.

17 ading to allergic pulmonary inflammation and airway hyperreactivity.

18 ergen-induced peribronchial inflammation and airway hyperreactivity.

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

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

21 o CRA-induced peribronchial inflammation and airway hyperreactivity.

22 evelopment of peribronchial inflammation and airway hyperreactivity.

23 hyperplasia, increased mucus secretion, and airway hyperreactivity.

24 increases acetylcholine release and leads to airway hyperreactivity.

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

26 and acceleration of severe allergen-induced airway hyperreactivity.

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

28 ll hyperplasia, and significantly attenuated airway hyperreactivity.

29 en, which induced pulmonary eosinophilia and airway hyperreactivity.

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

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

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

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

34 associated with the induction of reversible airway hyperreactivity.

35 interleukin-13 and interleukin-5 levels, and airway hyperreactivity.

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

37 eversible airflow obstruction resulting from airway hyperreactivity.

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

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

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

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

42 raviroc provided unique benefits in reducing airway hyperreactivity.

43 esis and ORMDL3 overexpression are linked to airway hyperreactivity.

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

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

46 aplasia, subepithelial fibrosis and enhanced airway hyperreactivity.

47 sensitization to environmental allergens and airway hyperreactivity.

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

49 nduction of allergic airway inflammation and airway hyperreactivity.

50 of alternatively activated macrophages, and airway hyperreactivity.

51 features of the allergic response including airway hyperreactivity.

52 population of neurons that are required for airway hyperreactivity.

53 y capacities and efficiently dampen allergic airway hyperreactivity.

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

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

56 om dermatitis resulted in increased allergic airway hyperreactivity.

57 hypersecretion, Th2 cytokine production, and airways hyperreactivity.

58 iving postnatally, but develop emphysema and airways hyperreactivity.

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

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

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

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

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

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

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

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

67 modulatory effects of CpG A in IL-33-induced airway hyperreactivity (AHR) and airway inflammation.

68 ronic inflammatory disorder characterized by airway hyperreactivity (AHR) and driven by T(H)2 cytokin

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

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

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

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

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

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

75 The influence of regulatory B cells on airway hyperreactivity (AHR) and remodeling in asthma is

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

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

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

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

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

81 9 strain induced significant dose-responsive airway hyperreactivity (AHR) in BALB/c mice at days 6 an

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 mAb and examined for airway inflammation and airway hyperreactivity (AHR), a cardinal feature of asth

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

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

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

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

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

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

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

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

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

107 immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophi

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

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

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

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

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

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

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

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

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

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

118 the mice as adults against allergen-induced airway hyperreactivity (AHR).

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

120 is a leading chronic disease associated with airway hyperreactivity (AHR).

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

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

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

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

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

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

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

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

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

130 (ACO) represents the confluence of bronchial airway hyperreactivity and chronic airflow limitation an

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

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

133 over, the ability of induced Treg to control airway hyperreactivity and effector functions of lung T

134 not Hutterite homes significantly inhibited airway hyperreactivity and eosinophilia.

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

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

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

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

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

140 Preterm infants can develop airway hyperreactivity and impaired bronchodilation foll

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

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

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

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

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

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

147 ntratracheally before Ag challenge mitigated airway hyperreactivity and inflammation.

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

149 Induction of airway hyperreactivity and lung inflammation increased l

150 then challenged with IL-33 and assessed for airway hyperreactivity and lung inflammation.

151 PE (days 13-15) followed by determination of airway hyperreactivity and lung T cell effector function

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

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

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

155 )-challenged Apoe(-/-) mice display enhanced airway hyperreactivity and mucous cell metaplasia.

156 13Ralpha1 was essential for allergen-induced airway hyperreactivity and mucus hypersecretion but not

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

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

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

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

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

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

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

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

165 Further, this subset dampens airway hyperreactivity and significantly reduces lung in

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

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

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

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

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

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

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

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

174 tly, allergen-induced IgE-dependent colitis, airway hyperreactivity, and mucus-producing goblet cells

175 Because AC and airway hyperreactivity are allergic diseases of mucosal

176 Airway tone and airway hyperreactivity are mediated by the parasympathet

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

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

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

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

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

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

183 doptive transfer to mice, and measurement of airway hyperreactivity by Flexivent.

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

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

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

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

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

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

190 The induction of airway hyperreactivity during allergic responses involve

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

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

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

194 evented the development of ovalbumin-induced airway hyperreactivity, eosinophilia, and goblet cell me

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

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

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

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

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

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

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

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

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

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

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

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

207 n-derived neurotrophic factor contributes to airway hyperreactivity in a mouse model of allergic asth

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

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

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

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

212 blocking of IFN-gamma activity, exacerbates airway hyperreactivity in allergen-challenged mice, prov

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

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

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

216 n of hypoferremia reduced the development of airway hyperreactivity in experimental models of ILC2-dr

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

218 i-CD52 antibody and reduces allergen-induced airway hyperreactivity in mice.

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

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

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

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

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

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

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

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

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

228 Having airway hyperreactivity increased the risk of rapid decli

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

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

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

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

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

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

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

236 Airway hyperreactivity, measured by the methacholine-pro

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

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

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

240 th channelrhodopsin dramatically exacerbates airway hyperreactivity of inflamed airways.

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

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

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

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

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

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

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

248 Airway hyperreactivity, recruitment of infiltrating cell

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

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

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

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

253 challenge and monitored by mini endoscopy or airway hyperreactivity, respectively.

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

255 The airway hyperreactivity response was significantly increa

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

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

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

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

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

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

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

263 Airway hyperreactivity that follows exposure to antigen

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

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

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

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

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

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

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

271 (40%) patients demonstrated some evidence of airway hyperreactivity to include eight who met asthma c

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

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

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

275 Airway hyperreactivity to methacholine observed on Day 7

276 Unexpectedly, airway hyperreactivity to methacholine was essentially a

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

278 of eosinophils, and MCTR3 potently decreased airway hyperreactivity to methacholine, bronchoalveolar

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

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

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

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

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

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

285 Reversible airway hyperreactivity underlies the pathophysiology of

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

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

288 Airway hyperreactivity was mediated by MCP-1 through CCR

289 Interestingly, airway hyperreactivity was significantly decreased at ea

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

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

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

293 , allergen-induced IgE-dependent colitis and airway hyperreactivity were also enhanced in ATI-fed mic

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

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

296 pulations expressed type 2 genes and induced airway hyperreactivity when adoptively transferred to mi

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

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

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

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