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1 hat involves airway hyper-responsiveness and mucus hypersecretion.
2 with the severity of airway inflammation and mucus hypersecretion.
3 esulting in increased airway eosinophils and mucus hypersecretion.
4 ion, goblet cell hyperplasia/metaplasia, and mucus hypersecretion.
5 hyperresponsiveness (AHR), inflammation, and mucus hypersecretion.
6 e associated with goblet cell metaplasia and mucus hypersecretion.
7 choconstriction, parenchymal destruction and mucus hypersecretion.
8 al implications for the management of airway mucus hypersecretion.
9 inflammatory airway diseases associated with mucus hypersecretion.
10 erbations, which are associated with further mucus hypersecretion.
11 ts for pharmacological intervention to treat mucus hypersecretion.
12 age fluid and airway tissue eosinophilia and mucus hypersecretion.
13 inophil infiltration, VCAM-1 expression, and mucus hypersecretion.
14 onses and increases viral titres, leading to mucus hypersecretion.
15 nhibitor NU7441 reduced airway eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OV
16 re, wild-type mice had chronic inflammation, mucus hypersecretion, airway remodeling, emphysema, and
17 irway disease characterized by inflammation, mucus hypersecretion and abnormal airway smooth muscle (
18  chronic airway inflammation, which leads to mucus hypersecretion and airway hyperresponsiveness.
19                Remodeling processes, such as mucus hypersecretion and extracellular matrix protein pr
20 strate that Lyn overexpression decreased the mucus hypersecretion and levels of the muc5ac transcript
21 ponse of the airways that is associated with mucus hypersecretion and obstruction of small airways.
22                                              Mucus hypersecretion and persistent airway inflammation
23 pha-deficient animals specifically inhibited mucus hypersecretion and reduced IL-13.
24 l infiltration, goblet cell hyperplasia with mucus hypersecretion, and accumulation and activation of
25 eactivity, eosinophilic airway inflammation, mucus hypersecretion, and Ag-specific Ig production.
26 nophilic inflammation, Th2 cytokine release, mucus hypersecretion, and AHR.
27 reduction in airway eosinophil infiltration, mucus hypersecretion, and airway hyperreactivity in resp
28 nal features of asthma: airway eosinophilia, mucus hypersecretion, and airway hyperreactivity.
29  characterized by eosinophilic inflammation, mucus hypersecretion, and airway hyperresponsiveness (AH
30 sease that is characterized by inflammation, mucus hypersecretion, and airway hyperresponsiveness.
31 airway hyperresponsiveness, gene expression, mucus hypersecretion, and airway inflammation was assess
32             However, goblet cell metaplasia, mucus hypersecretion, and airway obstruction are integra
33 t also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosis.
34 reased allergen-induced airway inflammation, mucus hypersecretion, and hyperresponsiveness in the hGX
35 associated with a reduction in eosinophilia, mucus hypersecretion, and IL-5 and IL-13 production upon
36 ve as a therapeutic target for inflammation, mucus hypersecretion, and structural lung damage and ind
37 ainst ovalbumin-induced airway eosinophilia, mucus hypersecretion, and Th2 cytokine production (IL-4/
38 leading to eosinophilic airway inflammation, mucus hypersecretion, and Th2 cytokine production in res
39 the development of AHR, airway eosinophilia, mucus hypersecretion, and TH2 cytokine production withou
40 racterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production.
41                   Eosinophil recruitment and mucus hypersecretion are characteristic of asthmatic air
42                   Goblet cell metaplasia and mucus hypersecretion are important features in the patho
43 A-induced inflammatory cell infiltration and mucus hypersecretion as observed in lung sections, and m
44 ungs were examined for cell infiltration and mucus hypersecretion, as well as the expression of antio
45 ncy also diminished goblet cell hyperplasia, mucus hypersecretion, bronchoalveolar lavage eosinophili
46  allergen-induced airway hyperreactivity and mucus hypersecretion but not for fibroblast or alternati
47               However, IL-6 is essential for mucus hypersecretion by airway epithelial cells triggere
48 ssibility that adenosine also contributes to mucus hypersecretion by airway epithelial cells.
49 d that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and its bi
50 monstrated that M. pneumoniae induces airway mucus hypersecretion by modulating the STAT/EGFR-FOXA2 s
51 tive Rho-A/Rho kinase inhibitor, affects the mucus hypersecretion by suppressing MUC5AC via signal tr
52 the mechanism by which M. pneumoniae induces mucus hypersecretion by using M. pneumoniae infection of
53                                      Chronic mucus hypersecretion (CMH) is common among smokers and i
54 ntly reduced airway eosinophil infiltration, mucus hypersecretion, edema, and IL-4 levels in a mouse
55 se, airway hyperreactivity, T(H)2 responses, mucus hypersecretion, eosinophil infiltration, and colla
56 ased bronchoalveolar lavage eosinophilia and mucus hypersecretion following the secondary challenge p
57 lar infiltration with concomitant epithelial mucus hypersecretion, goblet cell metaplasia, subepithel
58 TH2-mediated goblet cell differentiation and mucus hypersecretion in a murine model of allergic lung
59   However, its function in modulating airway mucus hypersecretion in asthma remains undefined.
60 hypersecretory drugs for treatment of airway mucus hypersecretion in asthma.
61 nd implicate NKCC1 in the pathophysiology of mucus hypersecretion in asthma.
62  airway inflammation and hyperreactivity and mucus hypersecretion in house dust mite-challenged mice.
63 ggest that propofol (Diprivan) may stimulate mucus hypersecretion in patients without pulmonary disea
64 mice, there was no goblet cell metaplasia or mucus hypersecretion in response to OVA, even in the pre
65  2 cytokine production in the peritoneum, or mucus hypersecretion in the gastrointestinal tract.
66 ant mediators of the eosinophilic influx and mucus hypersecretion in the lungs in a murine model of a
67  in diminished eosinophilic inflammation and mucus hypersecretion in the lungs of allergen-sensitized
68                                              Mucus hypersecretion is a common characteristic of asthm
69                                       Airway mucus hypersecretion is a feature of many patients with
70                                              Mucus hypersecretion is a hallmark of asthma that contri
71                                       Airway mucus hypersecretion is a key pathophysiologic feature i
72                                       Airway mucus hypersecretion is a key pathophysiological feature
73                                              Mucus hypersecretion is a prominent manifestation in pat
74                                              Mucus hypersecretion is a prominent manifestation in pat
75                                      Because mucus hypersecretion is common in purulent rhinitis, we
76 g events such as epithelial desquamation and mucus hypersecretion leading to airway obstruction, sube
77 e damage, inflammatory cell recruitment, and mucus hypersecretion may be associated with substantial
78 IL-11 did not cause a comparable decrease in mucus hypersecretion, Muc 5ac gene expression, or the le
79                      Airway inflammation and mucus hypersecretion/overproduction/obstruction are path
80 , which includes recruitment of eosinophils, mucus hypersecretion, Th2 cytokine production, and airwa
81 nflammation, airway hyperresponsiveness, and mucus hypersecretion to a similar degree as detected in
82  hyperresponsiveness, lung inflammation, and mucus hypersecretion to the degree observed in wild-type
83                                              Mucus hypersecretion upon Pofut1 inactivation is accompa
84 acterized by airway eosinophilia, as well as mucus hypersecretion, which can lead to airflow obstruct
85 lic inflammation, Th2 cell accumulation, and mucus hypersecretion with mucus metaplasia.
86  cell hypertrophy and hyperplasia as well as mucus hypersecretion with subsequent airflow obstruction
87 rly suppressed AHR, airway eosinophilia, and mucus hypersecretion without any reduction in TH2 cytoki

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