ライフサイエンスコーパス: airway mucus

1 ycoproteins, the principal macromolecules in airway mucus.

2 ight serve as therapeutic targets to control airway mucus.

3 rway mucus and identify agents that decrease airway mucus.

4 pe A receptors (GABA(A)Rs) are implicated in airway mucus.

5 ological sections confirmed that Dex reduced airway mucus.

6 mM nitrite (NO2) at pH 6.5, which mimics CF airway mucus.

7 uction of MUC5AC mucin, a major component of airway mucus.

8 lveolar enlargement and excess production of airway mucus.

9 expression were not significantly reduced by airway mucus.

10 fibrosis bronchiectasis is characterized by airway mucus accumulation and sputum production, but the

11 omputed tomography imaging abnormalities and airway mucus accumulation but not airway inflammation in

12 Levels of airway mucus, airway eosinophils, and peribronchial CD4+

13 uation of viral load, protein concentration, airway mucus, airway reactivity, or ILC2 numbers.

14 al disease (signified by formation of excess airway mucus and accumulation of M2-differentiating lung

15 manifestations now include drugs that target airway mucus and airway surface liquid hydration, and an

16 Here, we review the roles of airway mucus and CFTR in normal lung function, the previ

17 by which cigarette smoke/nicotine regulates airway mucus and identify agents that decrease airway mu

18 Methods: Airway mucus and mucins were evaluated in COVID-19 autop

19 reduced lung IL-13 protein levels, decreased airway mucus and reactivity, attenuated weight loss, and

20 pplemented with L. johnsonii exhibit reduced airway mucus and Th2 cell-mediated response to RSV infec

21 MUC5AC mucin is a major component of airway mucus, and its expression is modulated by a TNF-a

22 ane fusion processes, including secretion of airway mucus, antibody, insulin, gastric acids, and ions

23 vated levels of IL-13 and IL-5 and increased airway mucus at 20 days of age.

24 respiring anaerobically within the thickened airway mucus, at a pH of approximately 6.5.

25 11-3p, which could effectively penetrate the airway mucus barrier and deliver functional miR-511-3p t

26 er proteins is critical to better understand airway mucus biology and improve the management of lung

27 (concentrated) mucus in the CF lung impairs airway mucus clearance, which initiates bacterial infect

28 ies of in vitro binding to immobilized human airway mucus confirmed the inhibitory effect of encapsul

29 and epithelium, and the barrier function of airway mucus contribute significantly to this problem.

30 Abundant airway mucus contributes to airway obstruction in RSV di

31 CFTR(-/-) rat has revealed insights into the airway mucus defect characteristic of CF but does not re

32 ion, IgE levels, eosinophil recruitment, and airway mucus, demonstrating induction of allergic sensit

33 n of CFTR could result in the dehydration of airway mucus, depressing MC.

34 Airway glands, which produce most airway mucus, do so in response to both acetylcholine (A

35 smits by droplets generated from surfaces of airway mucus during processes of respiration within host

36 entify novel ways of preventing or reversing airway mucus dysfunction.

37 cystic fibrosis (CF) mucus ex vivo and mouse airway mucus ex situ.

38 ns, the primary macromolecular components of airway mucus, facilitate airway clearance by mucociliary

39 llergen- or nicotine/cigarette smoke-induced airway mucus formation in NHBE cells, murine airways, or

40 Nicotine-induced airway mucus formation is independent of IL-13, and alph

41 the allergen-induced mucous cell metaplasia, airway mucus formation, and the expression of mucus-rela

42 ological ligand for alpha7-nAChRs to trigger airway mucus formation.

43 Airway mucus forms the structural basis of the local inn

44 reby enabling the nanoparticles to cross the airway mucus gel layer and avoid phagocytic uptake by al

45 C5B, provide the organizing framework of the airways mucus gel and are major contributors to its rheo

46 The airways mucus gel performs a critical function in defend

47 of serum-specific IgE, cellular infiltrates, airway mucus goblet cells, and airway responsiveness wer

48 between fungal pneumonia and FOXA2-regulated airway mucus homeostasis.

49 tine and allergens are strong stimulators of airway mucus; however, the mechanism of mucus modulation

50 nstrated that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and

51 dies demonstrated that M. pneumoniae induces airway mucus hypersecretion by modulating the STAT/EGFR-

52 However, its function in modulating airway mucus hypersecretion in asthma remains undefined.

53 f anti-hypersecretory drugs for treatment of airway mucus hypersecretion in asthma.

54 Airway mucus hypersecretion is a feature of many patient

55 Airway mucus hypersecretion is a key pathophysiologic fe

56 Airway mucus hypersecretion is a key pathophysiological

57 clinical implications for the management of airway mucus hypersecretion.

58 -1 (ITLN-1) in the development of pathologic airway mucus in asthma.

59 on the physical and transport properties of airway mucus in spontaneously breathing dogs.

60 Airway mucus is a hallmark of respiratory syncytial viru

61 suggest that reducing the viscoelasticity of airway mucus is an achievable therapeutic goal with P300

62 Excessive airway mucus is an important cause of morbidity and mort

63 cent data indicate that cystic fibrosis (CF) airway mucus is anaerobic.

64 tration by 5%.Conclusions: Hyperconcentrated airway mucus is characteristic of subjects with bronchie

65 Airway mucus is composed of two mucins: mucin 5B (MUC5B)

66 Airway mucus is essential for lung defense, but excessiv

67 confirmed that Siglec-8 ligand on the human airway mucus layer is an isoform of DMBT1 carrying O-lin

68 Human upper airway mucus layer proteins were recovered during presur

69 ds and ducts are normally transported to the airway mucus layer, which is lost during tissue preparat

70 mphocyte recruitment were decreased, as were airway mucus, levels of specific proinflammatory mediato

71 mice had higher lung leukocyte counts, more airway mucus metaplasia, greater lung levels of some Th2

72 disease, the effects of these antagonists on airway mucus morphology were assessed in isolated perfus

73 s may be required for effective treatment of airway mucus obstruction in CF.

74 thogens, activate macrophages, contribute to airway mucus obstruction in cystic fibrosis, and facilit

75 ide a novel therapeutic target to ameliorate airway mucus obstruction in lung diseases.

76 nductance regulator, a Cl ion channel, cause airway mucus obstruction leading to fatal lung disease.

77 ological studies and cell counts revealed no airway mucus obstruction or inflammation in the lungs of

78 d that hypoxic epithelial necrosis caused by airway mucus obstruction precedes neutrophilic inflammat

79 h morbidity and mortality related to chronic airway mucus obstruction, inflammation, infection, and p

80 these data indicate that, in the context of airway mucus obstruction, the adaptive immune system sup

81 ns, treated Slc26a9-deficient mice exhibited airway mucus obstruction, which did not occur in wild-ty

82 anied by MCM, elevated MUC5B expression, and airway mucus obstruction.

83 radicable by antibiotics and responsible for airway mucus overproduction that contributes to airway o

84 In the thick CF airway mucus, P. aeruginosa forms antibiotic- and phagoc

85 Our results reveal genetic mechanisms of airway mucus pathobiology.

86 Airway mucus plays a critical role in clearing inhaled t

87 disease (COPD); however, the association of airway mucus plugging and mortality in patients with COP

88 abnormalities in lung morphology, including airway mucus plugging and wall thickening, in adolescent

89 Conclusion Airway mucus plugging at CT was associated with reduced

90 ed that may serve to identify occult central airway mucus plugging in the ventilated asthmatic patien

91 Lung segments with AT more frequently had airway mucus plugging than lung segments without AT (48%

92 l airspace enlargement, but had no effect on airway mucus plugging, bacterial infection, or pulmonary

93 formation of pathologic mucus which leads to airway mucus plugging.

94 Airway mucus plugs are common in patients with chronic o

95 Background Airway mucus plugs in asthma are associated with exacerb

96 In in vivo models of airway mucus plugs, neutrophil migration was inhibited b

97 Laboratory RSV strains differentially induce airway mucus production in mice.

98 henotype in experimental asthma with reduced airway mucus production, airway hyperresponsiveness and

99 ers, increased eosinophil apoptosis, reduced airway mucus production, and attenuated airway hyperresp

100 -induced airway inflammation, with increased airway mucus production, oxidative stress, inflammatory

101 bronchioalveolar lavage fluid, and enhanced airway mucus production.

102 peribronchiolar inflammation, and increased airway mucus production.

103 Blocking the chemokines also decreased airway mucus production.

104 a mice results from significant decreases in airway mucus production.

105 CTL inhibited eosinophil infiltration in the airway, mucus production, and cytokine accumulation in t

106 development of eosinophilic inflammation of airways, mucus production, and bronchial hyperreactivity

107 poxygenase-activating protein (FLAP) blocked airway mucus release and infiltration by eosinophils ind

108 nflux of eosinophils into the lungs, but not airway mucus release.

109 ns, but no approved or effective therapy for airway mucus retention in patients with chronic bronchit

110 ein level of lung IL-4, IL-5, and IL-13, and airway mucus score were also significantly decreased in

111 inflammatory, and infectious insults induce airway mucus secretion and goblet cell metaplasia to pre

112 everal downstream effects, including reduced airway mucus secretion and protection from endothelial b

113 The dominant neural control of human airway mucus secretion is cholinergic.

114 , rhinorrhea, coughing, bronchoconstriction, airway mucus secretion, dysphagia, altered gastrointesti

115 SL) hyperabsorption generates a concentrated airway mucus that interacts with P. aeruginosa to promot

116 the airways, cilia function in concert with airway mucus to mediate the critical function of mucocil

117 ance regulator (CFTR) leads to impairment of airway mucus transport and to chronic lung diseases resu

118 sity would contribute to the accumulation of airway mucus which is characteristic of this disease.