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1 ed by airway constriction, inflammation, and mucus hypersecretion.
2 ed NET formation, cellular inflammation, and mucus hypersecretion.
3 xygen species (ROS) production, NETosis, and mucus hypersecretion.
4 esulting in increased airway eosinophils and mucus hypersecretion.
5 onses and increases viral titres, leading to mucus hypersecretion.
6 hat involves airway hyper-responsiveness and mucus hypersecretion.
7 with the severity of airway inflammation and mucus hypersecretion.
8 ion, goblet cell hyperplasia/metaplasia, and mucus hypersecretion.
9 hyperresponsiveness (AHR), inflammation, and mucus hypersecretion.
10 e associated with goblet cell metaplasia and mucus hypersecretion.
11 choconstriction, parenchymal destruction and mucus hypersecretion.
12 al implications for the management of airway mucus hypersecretion.
13 inflammatory airway diseases associated with mucus hypersecretion.
14 erbations, which are associated with further mucus hypersecretion.
15 ts for pharmacological intervention to treat mucus hypersecretion.
16 age fluid and airway tissue eosinophilia and mucus hypersecretion.
17 inophil infiltration, VCAM-1 expression, and mucus hypersecretion.
18 nflammation, airway hyperresponsiveness, and mucus hypersecretion.
19                                   A detailed mucus hypersecretion adverse outcome pathway (AOP) has b
20 nhibitor NU7441 reduced airway eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OV
21 re, wild-type mice had chronic inflammation, mucus hypersecretion, airway remodeling, emphysema, and
22 irway disease characterized by inflammation, mucus hypersecretion and abnormal airway smooth muscle (
23  chronic airway inflammation, which leads to mucus hypersecretion and airway hyperresponsiveness.
24 and IL-13, airway hyperresponsiveness (AHR), mucus hypersecretion and eosinophilia.
25                Remodeling processes, such as mucus hypersecretion and extracellular matrix protein pr
26 on cellular functions such as proliferation, mucus hypersecretion and fibroblast differentiation in i
27 was assessed by airway hyper-responsiveness, mucus hypersecretion and inflammatory cell recruitment.
28 strate that Lyn overexpression decreased the mucus hypersecretion and levels of the muc5ac transcript
29 ponse of the airways that is associated with mucus hypersecretion and obstruction of small airways.
30                                              Mucus hypersecretion and persistent airway inflammation
31 pha-deficient animals specifically inhibited mucus hypersecretion and reduced IL-13.
32 l infiltration, goblet cell hyperplasia with mucus hypersecretion, and accumulation and activation of
33 eactivity, eosinophilic airway inflammation, mucus hypersecretion, and Ag-specific Ig production.
34 nophilic inflammation, Th2 cytokine release, mucus hypersecretion, and AHR.
35 reduction in airway eosinophil infiltration, mucus hypersecretion, and airway hyperreactivity in resp
36 nal features of asthma: airway eosinophilia, mucus hypersecretion, and airway hyperreactivity.
37  characterized by eosinophilic inflammation, mucus hypersecretion, and airway hyperresponsiveness (AH
38 sease that is characterized by inflammation, mucus hypersecretion, and airway hyperresponsiveness.
39 airway hyperresponsiveness, gene expression, mucus hypersecretion, and airway inflammation was assess
40             However, goblet cell metaplasia, mucus hypersecretion, and airway obstruction are integra
41 ology, including on airway epithelial cells, mucus hypersecretion, and airway remodelling, and conseq
42  signaling, extracellular matrix production, mucus hypersecretion, and eosinophil activation.
43 t also reduced airway hyperreactivity (AHR), mucus hypersecretion, and fibrosis.
44 rol Test scores, frequent history of chronic mucus hypersecretion, and frequent use of oral corticost
45 reased allergen-induced airway inflammation, mucus hypersecretion, and hyperresponsiveness in the hGX
46 associated with a reduction in eosinophilia, mucus hypersecretion, and IL-5 and IL-13 production upon
47                While inflammation, fibrosis, mucus hypersecretion, and metaplastic epithelial lesions
48 s activate ILC2s, resulting in eosinophilia, mucus hypersecretion, and remodeling of mucosal tissues.
49  inflammatory cell infiltrate and mediators, mucus hypersecretion, and serum total IgE.
50 ve as a therapeutic target for inflammation, mucus hypersecretion, and structural lung damage and ind
51 ainst ovalbumin-induced airway eosinophilia, mucus hypersecretion, and Th2 cytokine production (IL-4/
52 leading to eosinophilic airway inflammation, mucus hypersecretion, and Th2 cytokine production in res
53 the development of AHR, airway eosinophilia, mucus hypersecretion, and TH2 cytokine production withou
54 racterized by airway epithelial cell damage, mucus hypersecretion, and Th2 cytokine production.
55                   Eosinophil recruitment and mucus hypersecretion are characteristic of asthmatic air
56                   Goblet cell metaplasia and mucus hypersecretion are important features in the patho
57                     Chronic inflammation and mucus hypersecretion are key features of COPD.
58 gical agent would have therapeutic value for mucus hypersecretion as it is the major cause of airway
59 A-induced inflammatory cell infiltration and mucus hypersecretion as observed in lung sections, and m
60 ungs were examined for cell infiltration and mucus hypersecretion, as well as the expression of antio
61 ncy also diminished goblet cell hyperplasia, mucus hypersecretion, bronchoalveolar lavage eosinophili
62  allergen-induced airway hyperreactivity and mucus hypersecretion but not for fibroblast or alternati
63               However, IL-6 is essential for mucus hypersecretion by airway epithelial cells triggere
64 ssibility that adenosine also contributes to mucus hypersecretion by airway epithelial cells.
65 d that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and its bi
66 monstrated that M. pneumoniae induces airway mucus hypersecretion by modulating the STAT/EGFR-FOXA2 s
67 tive Rho-A/Rho kinase inhibitor, affects the mucus hypersecretion by suppressing MUC5AC via signal tr
68 the mechanism by which M. pneumoniae induces mucus hypersecretion by using M. pneumoniae infection of
69                                      Chronic mucus hypersecretion (CMH) is common among smokers and i
70                                              Mucus hypersecretion contributes to lung function impair
71 ntly reduced airway eosinophil infiltration, mucus hypersecretion, edema, and IL-4 levels in a mouse
72 se, airway hyperreactivity, T(H)2 responses, mucus hypersecretion, eosinophil infiltration, and colla
73 ased bronchoalveolar lavage eosinophilia and mucus hypersecretion following the secondary challenge p
74 lar infiltration with concomitant epithelial mucus hypersecretion, goblet cell metaplasia, subepithel
75 hmatics and reverses pathological effects of mucus hypersecretion in a mouse allergic asthma model.
76 TH2-mediated goblet cell differentiation and mucus hypersecretion in a murine model of allergic lung
77   However, its function in modulating airway mucus hypersecretion in asthma remains undefined.
78  developing treatments to inhibit effects of mucus hypersecretion in asthma.
79 hypersecretory drugs for treatment of airway mucus hypersecretion in asthma.
80 nd implicate NKCC1 in the pathophysiology of mucus hypersecretion in asthma.
81  airway inflammation and hyperreactivity and mucus hypersecretion in house dust mite-challenged mice.
82 ggest that propofol (Diprivan) may stimulate mucus hypersecretion in patients without pulmonary disea
83 mice, there was no goblet cell metaplasia or mucus hypersecretion in response to OVA, even in the pre
84  goblet cell hyperplasia and metaplasia, and mucus hypersecretion in the airways.
85  2 cytokine production in the peritoneum, or mucus hypersecretion in the gastrointestinal tract.
86 ant mediators of the eosinophilic influx and mucus hypersecretion in the lungs in a murine model of a
87  in diminished eosinophilic inflammation and mucus hypersecretion in the lungs of allergen-sensitized
88 e predictive of cigarette smoke exposure and mucus hypersecretion in vitro, and less conclusively pre
89                                              Mucus hypersecretion is a common characteristic of asthm
90                                       Airway mucus hypersecretion is a feature of many patients with
91                                              Mucus hypersecretion is a hallmark of asthma that contri
92                                       Airway mucus hypersecretion is a key pathophysiologic feature i
93                                       Airway mucus hypersecretion is a key pathophysiological feature
94                                              Mucus hypersecretion is a prominent manifestation in pat
95                                              Mucus hypersecretion is a prominent manifestation in pat
96                                      Because mucus hypersecretion is common in purulent rhinitis, we
97 g events such as epithelial desquamation and mucus hypersecretion leading to airway obstruction, sube
98 tions included downregulation of pathways of mucus hypersecretion, leukocyte migration/activation, an
99 oth sexes, as displayed by humoral response, mucus hypersecretion, lung inflammatory cell infiltratio
100 e damage, inflammatory cell recruitment, and mucus hypersecretion may be associated with substantial
101 urther understanding of the role of FOXA2 in mucus hypersecretion may lead to novel therapeutics agai
102 IL-11 did not cause a comparable decrease in mucus hypersecretion, Muc 5ac gene expression, or the le
103 ary nerves to decrease airway resistance and mucus hypersecretion.Objectives: To determine the safety
104                      Airway inflammation and mucus hypersecretion/overproduction/obstruction are path
105 , which includes recruitment of eosinophils, mucus hypersecretion, Th2 cytokine production, and airwa
106 nflammation, airway hyperresponsiveness, and mucus hypersecretion to a similar degree as detected in
107  hyperresponsiveness, lung inflammation, and mucus hypersecretion to the degree observed in wild-type
108                                              Mucus hypersecretion upon Pofut1 inactivation is accompa
109 acterized by airway eosinophilia, as well as mucus hypersecretion, which can lead to airflow obstruct
110 lic inflammation, Th2 cell accumulation, and mucus hypersecretion with mucus metaplasia.
111  cell hypertrophy and hyperplasia as well as mucus hypersecretion with subsequent airflow obstruction
112 rly suppressed AHR, airway eosinophilia, and mucus hypersecretion without any reduction in TH2 cytoki

 
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