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1 ion, which leads to mucus hypersecretion and airway hyperresponsiveness.
2 uced airway mucus production, and attenuated airway hyperresponsiveness.
3 ed mucus production together with pronounced airway hyperresponsiveness.
4 ormal lung function, and a greater degree of airway hyperresponsiveness.
5 ilic esophageal infiltration, and suppressed airway hyperresponsiveness.
6 n in airway inflammation, IgE Ab levels, and airway hyperresponsiveness.
7 (EIB) is a prototypical feature of indirect airway hyperresponsiveness.
8 ergic sensitization, airway inflammation and airway hyperresponsiveness.
9 haled air, blood and sputum eosinophils, and airway hyperresponsiveness.
10 zation prevented DEP-induced exacerbation of airway hyperresponsiveness.
11 by 82-96% (p </= 0.001) and fully normalized airway hyperresponsiveness.
12 acterized by chronic airway inflammation and airway hyperresponsiveness.
13 c pulmonary inflammation, and development of airway hyperresponsiveness.
14 associated with behavioral inhibition and/or airway hyperresponsiveness.
15 the therapeutic benefit of MSC treatment on airway hyperresponsiveness.
16 d cellular infiltration in BALF and allergic airway hyperresponsiveness.
17 and neutrophilic inflammation, but very mild airway hyperresponsiveness.
18 c effects on systemic allergic responses and airway hyperresponsiveness.
19 -13/GM-CSF) and a partial protection against airway hyperresponsiveness.
20 utically targeted to mitigate the effects of airway hyperresponsiveness.
21 ted, IL-13 increased airway inflammation and airway hyperresponsiveness.
22 reased neutrophils and IL-17, but equivalent airway hyperresponsiveness.
23 pes enhanced development of allergen-induced airway hyperresponsiveness.
24 These changes were independent from airway hyperresponsiveness.
25 ogical processes leading to inflammation and airway hyperresponsiveness.
26 hyperactivity, increased ASM contraction and airway hyperresponsiveness.
27 genes with atopy, asthma, atopic asthma, and airway hyperresponsiveness.
28 althy donors induced airway inflammation and airway hyperresponsiveness.
29 ted to the degree of airflow obstruction and airway hyperresponsiveness.
30 luding early and late pulses of IL-13 during airway hyperresponsiveness.
31 sion in airway smooth muscle cell (ASMC) and airway hyperresponsiveness.
32 bronchoalveolar lavage fluid, and increased airway hyperresponsiveness.
33 matrix can contribute to the development of airway hyperresponsiveness.
34 , we characterized the role of hyaluronan in airway hyperresponsiveness.
35 s in increased aeroantigen sensitization and airway hyperresponsiveness.
36 uppressed IL-1beta-induced steroid-resistant airway hyperresponsiveness.
37 cytokine levels, goblet cell metaplasia, and airway hyperresponsiveness.
38 ion, potentially promoting sensitization and airway hyperresponsiveness.
39 roid-resistant neutrophilic inflammation and airway hyperresponsiveness.
40 d by inflammation, mucus hypersecretion, and airway hyperresponsiveness.
41 ety and useful in the diagnosis of bronchial airway hyperresponsiveness.
42 cells, mucus production, and development of airways hyperresponsiveness.
43 hich causes persistent mucous metaplasia and airways hyperresponsiveness.
44 controls, virus-inoculated mice demonstrated airways hyperresponsiveness.
45 c, and fibrotic mediators and contributes to airways hyperresponsiveness.
46 ophilic inflammation, mucous metaplasia, and airways hyperresponsiveness.
47 the effect of imatinib, a KIT inhibitor, on airway hyperresponsiveness, a physiological marker of se
48 of type 2-related inflammation and change in airway hyperresponsiveness after 6 weeks of fluticasone
51 ions of S1P and SphK1 to mast cell-dependent airway hyperresponsiveness (AHR) and airway inflammation
53 hese BMDCs before allergen challenge induces airway hyperresponsiveness (AHR) and eosinophilic airway
54 enged mice induced Treg cells and attenuated airway hyperresponsiveness (AHR) and inflammation compar
55 nd on development of ovalbumin (OVA)-induced airway hyperresponsiveness (AHR) and inflammation in an
56 role in the development of allergen-induced airway hyperresponsiveness (AHR) and inflammation in mic
57 ntly demonstrated that IVIg protects against airway hyperresponsiveness (AHR) and inflammation in mou
59 is a complex human disease characterized by airway hyperresponsiveness (AHR) and inflammation, where
62 basal airway function, bacterial LPS-induced airway hyperresponsiveness (AHR) and lung inflammation,
63 B/c mice resulted in significantly increased airway hyperresponsiveness (AHR) and macrophage and neut
64 e (ASM) contractility and the development of airway hyperresponsiveness (AHR) are cardinal features o
65 ance and also increased methacholine-induced airway hyperresponsiveness (AHR) as measured by lung res
66 ls' (aSMCs) contraction and proliferation in airway hyperresponsiveness (AHR) associated with asthma
67 rway smooth muscle (ASM) plays a key role in airway hyperresponsiveness (AHR) but it is unclear wheth
68 Tgfbm3(C57) synergize to reverse accentuated airway hyperresponsiveness (AHR) caused by low TGFbeta1
69 cell (ILC) and TH2 cell numbers but similar airway hyperresponsiveness (AHR) compared with those aft
70 g surfactant protein A (SP-A) have increased airway hyperresponsiveness (AHR) during M pneumoniae inf
71 lic and neutrophilic airway inflammation and airway hyperresponsiveness (AHR) following allergen chal
72 ole of the Nlrp3 inflammasome in nonallergic airway hyperresponsiveness (AHR) has not previously been
73 the development of allergic inflammation and airway hyperresponsiveness (AHR) in acute murine models.
74 exposure results in greater inflammation and airway hyperresponsiveness (AHR) in obese versus lean mi
75 development of eosinophilic inflammation and airway hyperresponsiveness (AHR) in sensitized individua
76 e we demonstrate that IL-17A mediated severe airway hyperresponsiveness (AHR) in susceptible strains
77 is a wide variation among humans and mice in airway hyperresponsiveness (AHR) in the absence of aller
80 flammation and remodelling in the airway and airway hyperresponsiveness (AHR) to cholinergic stimuli,
82 VA-asthmatic mice, significant diminution of airway hyperresponsiveness (AHR) was first apparent, whe
83 taining objective evidence of athlete asthma/airway hyperresponsiveness (AHR) were collected for all
84 this mechanism may result in a reduction of airway hyperresponsiveness (AHR) when using triple thera
85 te that IL-21R-deficiency reduces HDM-driven airway hyperresponsiveness (AHR) with only partial effec
86 e subjected to this SA model failed to mount airway hyperresponsiveness (AHR) without appreciable eff
87 h2 asthma phenotype that is characterized by airway hyperresponsiveness (AHR) without eosinophilic in
88 r Aspergillus fumigatus (AF) extract-induced airway hyperresponsiveness (AHR), airway inflammation, i
89 Asthma is a chronic disease associated with airway hyperresponsiveness (AHR), airway obstruction and
90 ritical for preservation of allergen-induced airway hyperresponsiveness (AHR), airway resistance, and
91 isease characterized by airflow obstruction, airway hyperresponsiveness (AHR), and airway inflammatio
92 evaluate inflammation, NF-kappaB activation, airway hyperresponsiveness (AHR), and airway remodeling.
93 nt, namely, reductions in mucous metaplasia, airway hyperresponsiveness (AHR), and inflammatory cells
94 ere exposed to ozone, and lung inflammation, airway hyperresponsiveness (AHR), and mitochondrial func
95 m cells (MSCs) decrease airway eosinophilia, airway hyperresponsiveness (AHR), and remodelling in mur
96 pendent domains labelled from A to E, namely airway hyperresponsiveness (AHR), bronchitis, cough refl
97 y-eight hours after the final OVA challenge, airway hyperresponsiveness (AHR), bronchoalveolar fluid
99 Major features of allergic asthma include airway hyperresponsiveness (AHR), eosinophilic inflammat
100 ng with an aerosolized antagonist attenuates airway hyperresponsiveness (AHR), eosinophilic inflammat
101 terogeneity is an independent determinant of airway hyperresponsiveness (AHR), improves with bronchod
103 one, additional treatment with sGARP reduced airway hyperresponsiveness (AHR), influx of neutrophils
104 ed the role of IL-13 and IL-17A in mediating airway hyperresponsiveness (AHR), lung inflammation, and
105 allenged wild type mice displayed a striking airway hyperresponsiveness (AHR), mMCP-6(-/-) mice had l
106 In contrast to the anticipated reduction in airway hyperresponsiveness (AHR), OVA allergen-challenge
107 llergic asthma, it is not a prerequisite for airway hyperresponsiveness (AHR), suggesting that underl
108 nctions and mechanisms of RGS2 in regulating airway hyperresponsiveness (AHR), the pathophysiologic h
109 lates allergic airway inflammation (AAI) and airway hyperresponsiveness (AHR), we compared AAI and AH
110 models of O3-induced airway inflammation and airway hyperresponsiveness (AHR), we sought to investiga
118 evidence suggests that IL-17 contributes to airway hyperresponsiveness (AHR); however, the mechanism
120 hronic inflammatory disease characterized by airways hyperresponsiveness (AHR), reversible airflow ob
121 enotype was determined by the measurement of airway hyperresponsiveness, airway inflammation, and cyt
122 ltration, excessive Th2 polarization, marked airway hyperresponsiveness, alveolar simplification, dec
123 nflammasome inhibition using CRID3 prevented airway hyperresponsiveness and airway inflammation (both
125 tly suppressed RSV-induced steroid-resistant airway hyperresponsiveness and airway inflammation.
126 PGE(2) generation in the lung predisposes to airway hyperresponsiveness and aspirin intolerance in as
127 not CD4+ICOS-, cells inhibited BPEx-induced airway hyperresponsiveness and bronchoalveolar lavage eo
129 mice had an increased propensity to develop airway hyperresponsiveness and displayed significantly e
132 phenotype of BALB Cftr(tm1UNC) mice includes airway hyperresponsiveness and increased lymphocyte numb
133 f rest, a single exposure to HDM resulted in airway hyperresponsiveness and increased TH2 cytokine le
135 Exposure to respiratory allergens triggers airway hyperresponsiveness and inflammation characterize
136 terium leprae HSP65 prevented development of airway hyperresponsiveness and inflammation in mice.
138 elivery of anti-IFN-gamma antibodies induced airway hyperresponsiveness and inflammation in wild-type
139 s, HSP65-induced effects on allergen-induced airway hyperresponsiveness and inflammation were associa
140 s, is pivotal in the development of allergic airway hyperresponsiveness and inflammation, and yet rem
141 diated wild-type (WT) recipients exacerbates airway hyperresponsiveness and inflammation, whereas tra
144 may potently induce bronchial constriction, airway hyperresponsiveness and inflammatory cell influx
145 irways in vivo, such as bronchoconstriction, airway hyperresponsiveness and inflammatory cell influx
146 posure to Neu5Gc in mice resulted in reduced airway hyperresponsiveness and inflammatory cell recruit
151 -/-) mice were resistant to the induction of airway hyperresponsiveness and manifested improved lung
152 sal AM completely attenuated the OVA-induced airway hyperresponsiveness and mucosal plasma leakage bu
153 ed in ROCK2(+/-) vs. wild-type mice, as were airway hyperresponsiveness and mucous hypersecretion.
155 en-induced pathogenic consequences including airway hyperresponsiveness and mucus production via incr
156 placebo on either methacholine or histamine airway hyperresponsiveness and no change in ACQ or AQLQ.
157 terparts, pAgs triggered markedly heightened airway hyperresponsiveness and pulmonary eosinophilia in
158 orted that NQO1-null mice are protected from airway hyperresponsiveness and pulmonary inflammation fo
160 gp120 prior to allergen challenge abrogated airway hyperresponsiveness and reduced the inflammatory
163 terferon levels were associated with greater airway hyperresponsiveness and skin prick test response
164 tion prevented the subsequent enhancement of airway hyperresponsiveness and the development of airway
165 In mice, periostin is required for maximal airways hyperresponsiveness and inflammation after HDM s
166 haracterized by variable airway obstruction, airway hyperresponsiveness, and airway inflammation.
167 V-induced mucous metaplasia, ILC2 expansion, airway hyperresponsiveness, and epithelial cell IL-25 ex
168 C2 numbers, TH2 cell numbers and activation, airway hyperresponsiveness, and expression of the transc
169 d from allergen-induced tissue inflammation, airway hyperresponsiveness, and goblet cell metaplasia i
170 used epithelial desquamation, bronchiolitis, airway hyperresponsiveness, and increased breathing effo
171 the relationship among airway inflammation, airway hyperresponsiveness, and lung function is poorly
172 uction, which promoted chronic inflammation, airway hyperresponsiveness, and mucus production during
174 ess atopic sensitization, a lesser degree of airway hyperresponsiveness, and no concomitant allergic
175 monary inflammation, mucous cell metaplasia, airway hyperresponsiveness, and OVA-specific IgE compare
176 d airway eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OVA-specific IgE product
177 philic inflammation, goblet cell metaplasia, airway hyperresponsiveness, and progression of emphysema
178 bition reduced allergic airway inflammation, airway hyperresponsiveness, and pulmonary collagen depos
179 infection with respiratory syncytial virus, airway hyperresponsiveness, and severe bronchopulmonary
180 ly related to both behavioral inhibition and airway hyperresponsiveness, and so could not mediate the
181 nto the lung, IgE production, development of airway hyperresponsiveness, and Th2 T cell priming.
182 terized by increased goblet cell metaplasia, airway hyperresponsiveness, and Th2-mediated inflammatio
183 helium is a critical determinant of indirect airway hyperresponsiveness, and the airway epithelium mi
184 lationship between behavioral inhibition and airway hyperresponsiveness, and whether hormonal and imm
188 ug significantly attenuated allergen-induced airway hyperresponsiveness at 24 hours after allergen ch
189 s for FEV1, smaller bronchodilator response, airway hyperresponsiveness at baseline, and male sex wer
190 opathologic condition, mucus production, and airway hyperresponsiveness between wild-type and Nlrp3(-
191 rization with H. pylori extract prevents the airway hyperresponsiveness, bronchoalveolar eosinophilia
193 ition in rhesus monkeys (Macaca mulatta) and airway hyperresponsiveness, but not atopy, and the sugge
194 llenge test (MCT) is commonly used to assess airway hyperresponsiveness, but the diagnostic character
195 eals that PAR(2) activation protects against airway hyperresponsiveness by an unknown mechanism, poss
198 IG markedly improves ovalbumin (OVA)-induced airway hyperresponsiveness characterized by 4- to 6-fold
199 DEP and HDM coexposure markedly enhanced airway hyperresponsiveness compared with HDM exposure al
200 d TH2 cells, type 2 cytokine production, and airway hyperresponsiveness compared with sole DEPs or HD
201 Serum allergen-specific antibody levels, airway hyperresponsiveness, cytokine levels in spleen ce
203 FAO significantly decreased allergen-induced airway hyperresponsiveness, decreased the number of infl
204 with poorly controlled severe asthma who had airway hyperresponsiveness despite receiving maximal med
205 lphavbeta6-deficient mice are protected from airway hyperresponsiveness, due in part to increased exp
207 med at various time points for evaluation of airway hyperresponsiveness, eosinophilia, mucus producti
208 bited hallmark features of asthma, including airway hyperresponsiveness, eosinophilic accumulation, a
209 nced responses to ozone, including increased airway hyperresponsiveness, exacerbated neutrophil influ
210 3A suppresses Th2 pulmonary inflammation and airway hyperresponsiveness following aeroallergen exposu
212 rway hyperresponsiveness; however, at 7 days airway hyperresponsiveness had completely resolved in Da
213 yc (iPSC-w/o-c-Myc) in allergic diseases and airway hyperresponsiveness has not been investigated.
214 At 24 hours, Darc(E2) mice had increased airway hyperresponsiveness; however, at 7 days airway hy
215 ed tissue ATP levels explain protection from airway hyperresponsiveness, i.e., absence of COX4i2 lead
217 valbumin from those of airway remodeling and airway hyperresponsiveness, illustrating independent gen
218 Ab production, type 2 cytokine response, and airway hyperresponsiveness in 4 wk, followed by airway r
219 lic lung inflammation, mucus production, and airway hyperresponsiveness in an experimental model of O
220 s the development of airway inflammation and airway hyperresponsiveness in an experimental murine mod
223 GF factor 8 (Mfge8(-/-)) develop exaggerated airway hyperresponsiveness in experimental models of ast
224 acetate modulates allergic inflammation and airway hyperresponsiveness in human atopic asthmatics in
226 f type 2 cytokines, airway eosinophilia, and airway hyperresponsiveness in juvenile Scnn1b-Tg mice.
227 treatment had no effect on inflammation and airway hyperresponsiveness in mice that received CD25-de
228 Both BAY 41-2272 and BAY 60-2770 reversed airway hyperresponsiveness in mice with allergic asthma
229 eosinophilic airway infiltration as well as airway hyperresponsiveness in mouse models of Ag-induced
230 lung fibrosis, smooth muscle hyperplasia and airway hyperresponsiveness in mouse models of chronic as
231 rsed IgE and TH2 cytokine production but not airway hyperresponsiveness in OVA-challenged DNA-PKcs(+/
233 and inhibition of GSNO reductase attenuated airway hyperresponsiveness in vivo among juvenile and ad
234 K(d) = 2 microM and significantly attenuates airways hyperresponsiveness in a murine model of allergi
235 ed allergic responses and the development of airway hyperresponsiveness, in part, through Act1's func
236 RNA-treated mice produced significantly less airway hyperresponsiveness induced by methacholine.
238 IL-17A production and substantially reduced airway hyperresponsiveness, inflammation, and lung funga
240 ced asthma exhibited substantially increased airway hyperresponsiveness, inflammation, and remodeling
241 m lungs of naive mice regulate lung allergic airway hyperresponsiveness, inflammation, levels of Th2
242 bination for 8 consecutive days, after which airway hyperresponsiveness, inflammatory cell influx int
244 c mice results in a dramatic upregulation of airway hyperresponsiveness, lung resistance, and TH2 res
245 ferences were noted between the 2 sexes with airway hyperresponsiveness (mannitol provocation testing
246 ients with severe asthma, imatinib decreased airway hyperresponsiveness, mast-cell counts, and trypta
247 The primary end point was the change in airway hyperresponsiveness, measured as the concentratio
250 of inhaled corticosteroids, had more severe airway hyperresponsiveness, more often nasal polyps, and
252 roxia induced asthma-like features including airway hyperresponsiveness, mucus hyperplasia, airway eo
253 ce results in increased lung granulocytosis, airway hyperresponsiveness, mucus overproduction, collag
254 se exposed to IL-13 and IL-17A had augmented airway hyperresponsiveness, mucus production, airway inf
255 gether, PTX3 deficiency results in augmented airway hyperresponsiveness, mucus production, and IL-17A
256 features of disease in our model, including airway hyperresponsiveness, neutrophilic and eosinophili
257 lvement in long-term airway inflammation and airway hyperresponsiveness occurred at least partially v
259 ma have not been able to show a reduction in airway hyperresponsiveness or change in FEV(1) but have
260 nset of TH2 immune responses and OVA-induced airway hyperresponsiveness or goblet cell hyperplasia, i
261 tic recipients by </= 23% but did not affect airway hyperresponsiveness or IgE levels, whereas equal
262 with only OVA Ag were sufficient to trigger airway hyperresponsiveness, prominent eosinophilic infla
263 genes (FAM129A, SYNPO2) were associated with airway hyperresponsiveness (provocative concentration of
264 methasone (DEX) in counteracting OVA-induced airway hyperresponsiveness, recruitment of eosinophils,
265 ing and deep inspirations (DI) in modulating airway hyperresponsiveness remains poorly understood.
266 ils deficient in IL-13 were unable to rescue airway hyperresponsiveness, T cell recruitment to the lu
270 t mice are protected from the development of airway hyperresponsiveness, Th2 cytokine production, eos
271 airway mucin expression levels, and greater airway hyperresponsiveness than infection with rA2-A2F o
272 ot mature mice, causes mucous metaplasia and airway hyperresponsiveness that are associated with the
273 s associated with lung function deficits and airways hyperresponsiveness that appear to be establishe
274 nt randomization, imatinib treatment reduced airway hyperresponsiveness to a greater extent than did
276 humoral and cellular immunological profiles, airway hyperresponsiveness to bronchospastic stimuli, an
278 ) mice that were exposed to Cl2 demonstrated airway hyperresponsiveness to inhaled methacholine signi
280 hy, sputum cell count, exhaled nitric oxide, airway hyperresponsiveness to mannitol, respiratory syst
281 equently challenged with ovalbumin exhibited airway hyperresponsiveness to methacholine aerosol and i
283 zed to and challenged with OVA had increased airway hyperresponsiveness to methacholine challenge and
284 BALB Cftr(tm1UNC) mice presented an enhanced airway hyperresponsiveness to methacholine challenge com
285 evels of fractional exhaled nitric oxide and airway hyperresponsiveness to methacholine were not affe
289 on to that antigen, in the form of increased airway hyperresponsiveness upon a later challenge, where
292 levels were higher in CysLTr1(-/-) mice and airway hyperresponsiveness was ameliorated using a granu
293 ce were challenged with aerosols to HDM, and airway hyperresponsiveness was evaluated by using plethy
294 response in OVA-challenged WT mice, although airway hyperresponsiveness was greater in Stard7(+/-) re
296 d did not reduce remodeling or IL-33 levels; airway hyperresponsiveness was only partially reduced.
297 portantly, chronic allergic inflammation and airway hyperresponsiveness were dependent on IL-4Ralpha-
299 t cell hyperplasia, collagen deposition, and airway hyperresponsiveness were significantly diminished
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