ライフサイエンスコーパス: mucus production

1 te, potentially due to the energetic cost of mucus production.

2 results from significant decreases in airway mucus production.

3 hypertension, pain, diarrhea, and excessive mucus production.

4 by significant increases in inflammation and mucus production.

5 , inflammation, levels of Th2 cytokines, and mucus production.

6 cialized and nonredundant role in intestinal mucus production.

7 e revealed no enhancement of inflammation or mucus production.

8 of disease by IL-22 was mediated by enhanced mucus production.

9 he accumulation of eosinophils and augmented mucus production.

10 lar epithelial cells staining positively for mucus production.

11 orrelated with reduction in allergen-induced mucus production.

12 production, airway hyperresponsiveness, and mucus production.

13 y completely protected from allergen-induced mucus production.

14 immunity may play a role in asbestos-induced mucus production.

15 deling, including peribronchial fibrosis and mucus production.

16 ntagonist, prevented airway eosinophilia and mucus production.

17 tributes to the severity of inflammation and mucus production.

18 way responsiveness, tissue eosinophilia, and mucus production.

19 educed airway eosinophilia without affecting mucus production.

20 pletely abolished both lung inflammation and mucus production.

21 d decreases in IgE titers as well as reduced mucus production.

22 airways were epithelial cell hypertrophy and mucus production.

23 helial cell damage and sloughing, along with mucus production.

24 issect further the mechanisms of Th2-induced mucus production.

25 rance occurred that was potentially aided by mucus production.

26 tically important in Th2 cell stimulation of mucus production.

27 of asthma, including airway eosinophilia and mucus production.

28 Th1 and Th2 cells in airway inflammation and mucus production.

29 not recruited to the lung and did not induce mucus production.

30 n of inflammation, but has no direct role in mucus production.

31 ociated FOXP3 gene expression, and increased mucus production.

32 pha1 antitrypsin, and FOXP4, an inhibitor of mucus production.

33 ioalveolar lavage fluid, and enhanced airway mucus production.

34 eosinophils and lymphocytes, and aggravated mucus production.

35 onchiolar inflammation, and increased airway mucus production.

36 hey regulate goblet cell differentiation and mucus production.

37 d expression of a network of genes mediating mucus production.

38 ution of the papain-induced eosinophilia and mucus production.

39 nflammation, airway hyperresponsiveness, and mucus production.

40 known to induce eosinophil accumulation and mucus production.

41 overexpression of memIL-13Ralpha2 increased mucus production.

42 locking the chemokines also decreased airway mucus production.

43 inophilic airway inflammation, serum IgE, or mucus production.

44 cell hyper/metaplasia, leading to increased mucus production.

45 airway inflammation in these diseases affect mucus production?

46 psy were used for morphometry evaluations of mucus production, airway epithelial thickening, perivasc

47 Mucus production, airway hyperresponsiveness to methacho

48 capable of inducing inflammation, excessive mucus production, airway hyperresponsiveness, alveolar r

49 7A had augmented airway hyperresponsiveness, mucus production, airway inflammation, and IL-13-induced

50 f RSV bronchiolitis, since it contributes to mucus production and airway hyperreactivity in our model

51 n peroxide serves a role in suppressing both mucus production and airway hyperresponsiveness.

52 rexpression of IL-25 by these cells leads to mucus production and airway infiltration of macrophages

53 We included RSV r19F because it induces mucus production and airway resistance, two manifestatio

54 immune responses and demonstrated increased mucus production and amplified cytokine responses in the

55 e (CS) exposure is associated with increased mucus production and chronic obstructive pulmonary disea

56 mpaired immunity was associated with reduced mucus production and decreased intestinal expression of

57 a chronic inflammatory state with increased mucus production and decreased lung function.

58 se studies establish a role for Th2 cells in mucus production and dissect the effector functions of I

59 L-13 markedly inhibits allergen-induced AHR, mucus production and eosinophilia.

60 IL-4, IL-13 may be critical for Th2-induced mucus production and eosinophilia.

61 Mucus production and epithelial integrity was assessed i

62 s associated with a significant reduction in mucus production and goblet cell metaplasia in these mic

63 of host resistance but that gastrointestinal mucus production and hemostasis pathways may also play a

64 ized by eosinophilic pulmonary inflammation, mucus production and reversible airway obstruction.

65 anges in the airways, including intraluminal mucus production and subepithelial collagen deposition,

66 nificantly reduced eosinophilia, IgE levels, mucus production and Th2 cytokines, while free CpG had o

67 n the exacerbated disease, including reduced mucus production and Th2 cytokines, with decreased viral

68 loride channel involved in the regulation of mucus production and/or secretion.

69 Persistent airway inflammation, mucus production, and airway hyperreactivity are the maj

70 s, bronchoalveolar lavage fluid eosinophils, mucus production, and airway hyperreactivity.

71 way eosinophilia, histopathologic condition, mucus production, and airway hyperresponsiveness between

72 neutrophilic/eosinophilic lung inflammation, mucus production, and airway hyperresponsiveness in an e

73 ed in an increase in airway hyperreactivity, mucus production, and airway inflammation (eosinophilia)

74 hown to cause bronchoconstriction, increased mucus production, and airway inflammation, three critica

75 Airway inflammation, cytokine expression, mucus production, and airway reactivity was assessed in

76 s, pulmonary inflammatory cell infiltration, mucus production, and airway resistance after challenge.

77 tration in the airways, reduced cytokine and mucus production, and almost completely abolished airway

78 creased eosinophil apoptosis, reduced airway mucus production, and attenuated airway hyperresponsiven

79 ent of eosinophilic inflammation of airways, mucus production, and bronchial hyperreactivity in a mou

80 bited eosinophil infiltration in the airway, mucus production, and cytokine accumulation in the bronc

81 d DCs induced a similar airway inflammation, mucus production, and cytokine production, but IgE or HD

82 on, including recruitment of CD4(+) T cells, mucus production, and development of airways hyperrespon

83 on TGF-beta and promotes epithelial damage, mucus production, and eosinophilia.

84 included eosinophilic infiltrates, increased mucus production, and epithelial cell hyperplasia/hypert

85 pression is responsible for the reduced AHR, mucus production, and fibrosis in BALB/c IL-10(-/-) mice

86 for IL-13Ralpha2 in the suppression of AHR, mucus production, and fibrosis.

87 as an increase in airway hyperreactivity and mucus production, and goblet cell hypertrophy.

88 emokine production, and airway eosinophilia, mucus production, and hyperresponsiveness seen in Stat6(

89 hyperresponsiveness, eosinophil activation, mucus production, and IgE secretion.

90 Airway eosinophilia, mucus production, and IgE synthesis, all key features of

91 lts in augmented airway hyperresponsiveness, mucus production, and IL-17A-dominant pulmonary inflamma

92 n lung neutrophils, lymphomononuclear cells, mucus production, and inflammatory cytokines.

93 lung tissue were examined for inflammation, mucus production, and inflammatory mediator production.

94 ung, airway epithelial cell hypertrophy with mucus production, and mast cell hyperplasia, similar to

95 , including epithelial junctional complexes, mucus production, and mucosa-derived antimicrobials.

96 haracterized by bacterial infections, excess mucus production, and robust neutrophil recruitment.

97 parenchymal inflammation, airway epithelial mucus production, and serum allergen-specific IgE and al

98 ted directly with viral titers, temperature, mucus production, and symptom scores.

99 in the airways and pulmonary blood vessels, mucus production, and Th2 cytokine production.

100 nificantly decreased airway hyperreactivity, mucus production, and Th2 cytokines.

101 rescue IL-13-induced AHR, inflammation, and mucus production, and transgenic overexpression in WT mi

102 ells, and goblet cell hyperplasia and excess mucus production are central to the pathogenesis of chro

103 ting whether goblet cell (GC) metaplasia and mucus production are differentially regulated in proxima

104 precise molecular mechanisms for pathogenic mucus production are largely undetermined.

105 the signal transduction pathways leading to mucus production are poorly understood.

106 er and validate a new pathway for regulating mucus production as well as a corresponding therapeutic

107 nophils, CD4(+) lymphocyte infiltration, and mucus production, as well as depressed levels of CCL2 ch

108 airway resistance, strong Th2 cytokine, and mucus production, as well as mixed eosinophilic and neur

109 s aeroallergen-induced airway resistance and mucus production but not IgE and Th2 cytokine production

110 attenuated the IL-13-induced differentiation/mucus production by 67%.

111 ripts in their lungs and exhibited increased mucus production by airway epithelial cells in an IL-17-

112 Excessive mucus production by airway epithelium is a major charact

113 airway resistance and significantly enhanced mucus production by goblet cells concomitant with increa

114 Mucus production by goblet cells of the large intestine

115 The blockade of eosinophilia and mucus production by IFN-gamma likely occurs through diff

116 Impaired mucus production caused by IL-6 deficiency correlates wi

117 nic airway remodeling, including exacerbated mucus production, collagen deposition, dysregulated cyto

118 SV) mice had more abundant airway epithelial mucus production compared with OVA mice 14 days after in

119 -alpha(-/-) or TNF-R(-/-) MCs have decreased mucus production compared with that seen in mice engraft

120 smooth muscle layer, and reduced epithelial mucus production compared with WT mice.

121 a and inflammation (decreased Th2 cytokines, mucus production) compared with WT counterparts, attribu

122 Inverted ALIs exhibit beating cilia and mucus production, consistent with conventional ALIs, as

123 uman asthmatics and in animal models, excess mucus production correlates with airway eosinophilia.

124 e marked effect PARP-1 inhibition exerted on mucus production corroborated the effects observed on th

125 ot transforming growth factor-alpha, induced mucus production dependent on IKKbeta-mediated NF-kappaB

126 sitive correlation with body weight, whereas mucus production did not change with obesity.

127 activated in the lungs of humans with excess mucus production due to COPD.

128 nflammation, airway hyperresponsiveness, and mucus production during house dust mite-induced allergic

129 t mice resulted in significant inhibition of mucus production during RSV infection.

130 airway inflammation, hyperresponsiveness and mucus production during the effector phase of allergic a

131 ice was characterized by increased pulmonary mucus production, elevated serum IgE, and leukocyte airw

132 d exacerbated lung pathology, with increased mucus production, elevated viral load, and enhanced Th2

133 Increased mucus production evident at day 2 p.i. was concordant wi

134 of vagal tone and a consequent reduction in mucus production from submucosal glands and bronchodilat

135 n exacerbated RSV-induced disease pathology, mucus production, group 2 innate lymphoid cell infiltrat

136 irway eosinophilia, type 2 cytokine release, mucus production, high levels of serum IgE, and airway r

137 termine whether eosinophils are important in mucus production, IL-5-/- Th2 cells were transferred int

138 vage (BAL) fluid eosinophilia, and increased mucus production in a murine model of OVA-induced allerg

139 ortant role of IKKbeta in TNF-alpha-mediated mucus production in airway epithelium in vitro and in vi

140 compliance and tissue elastance) and reduced mucus production in airways.

141 irway hyperresponsiveness, inflammation, and mucus production in allergen-treated ST2 KO mice.

142 he A(3)R in regulating lung eosinophilia and mucus production in an environment of elevated adenosine

143 with OVA resulted in airway inflammation and mucus production in animals that received either poly(I:

144 Increased mucus production in asthma is an important cause of airf

145 Airway inflammation is believed to stimulate mucus production in asthmatic patients.

146 vate IL-13R and EGFR and are responsible for mucus production in both protective immune responses and

147 MAPK13 that is responsible for IL-13-driven mucus production in human airway epithelial cells.

148 h nanomolar potency that effectively reduced mucus production in human airway epithelial cells.

149 have documented that Pneumocystis increases mucus production in infant lungs, and animal models reve

150 local and systemic Th2 cytokine levels, and mucus production in lung bronchioles of mice, whereas in

151 es and Muc5ac expression and also attenuated mucus production in lung epithelial cells.

152 Additionally, there was a marked increase in mucus production in mice that received Th2 cells and inh

153 ory RSV strains differentially induce airway mucus production in mice.

154 the impairment of eosinophil recruitment and mucus production in OVA-challenged PARP-1(-/-) mice.

155 irway mucous cell metaplasia/hyperplasia and mucus production in response to various promucoid agents

156 lls was sufficient for IL-13-induced AHR and mucus production in the absence of inflammation, fibrosi

157 lara cells are required for allergen-induced mucus production in the airway epithelium.

158 -induced expression of CD23 as well as lower mucus production in the airway epithelium.

159 ice further enhanced Th2 immune response and mucus production in the airways during respiratory syncy

160 - mice demonstrated significant increases in mucus production in the airways of RSV-infected mice.

161 argement of alveolar spaces and increases in mucus production in the bronchial airways.

162 ced effector T cell responses and pathogenic mucus production in the lung after RSV infection.

163 bition of eosinophil infiltration and excess mucus production in the lung, decreased levels of Th2 cy

164 a potential therapeutic agent for inhibiting mucus production in the pathogenesis of OM.

165 g, and inhibition of IL-13 abolished AHR and mucus production in these mice.

166 TNF-alpha-induced mucus production in vivo could also be inhibited by admi

167 loride channel involved in the regulation of mucus production, in primary murine airway epithelial ce

168 ic IL-4 production, airway eosinophilia, and mucus production, increased IFN-gamma production, and pr

169 ave both been implicated in allergen-induced mucus production, inflammation, and airway hyperreactivi

170 of airway hyperresponsiveness, eosinophilia, mucus production, inflammatory gene expression, and TH a

171 Increased mucus production is a common cause of morbidity and mort

172 Increased mucus production is a critical factor impairing lung fun

173 Excessive mucus production is an important pathological feature of

174 way biopsies of asthmatics but their role in mucus production is not clear.

175 ficult to determine whether allergen-induced mucus production is strictly dependent on direct effects

176 ding an 80-90% reduction in eosinophilia and mucus production, less goblet cell hyperplasia, and sign

177 on, and these findings suggest that enhanced mucus production may occur independently of BAL fluid eo

178 ction combined with allergic inflammation on mucus production may partially explain the more severe d

179 ommon adverse events reported were increased mucus production (montelukast, n=6; placebo, n=2), gastr

180 have identified new regulatory pathways for mucus production; mucus can be induced by Th2 and non-Th

181 hroat, cough, and headache and reduced nasal mucus production, nasal tissue use, and virus concentrat

182 h RV1B showed no change in IL-13 expression, mucus production, or airways responsiveness 28 d postinf

183 in airway epithelium that lead to increased mucus production, ovalbumin-sensitized and -challenged m

184 d airway inflammation, with increased airway mucus production, oxidative stress, inflammatory cell in

185 shedding in nasal secretions (P<.001), nasal mucus production (P=.004), and total respiratory illness

186 d deterioration of lung function, aggravated mucus production, peri-vascular, peri-bronchial, and all

187 acterized by recurrent episodes of wheezing, mucus production, pulmonary infiltrates, and elevated le

188 tiple alterations within the lung, including mucus production, recruitment of inflammatory cells, and

189 veness (AHR), eosinophilic inflammation, and mucus-production responses to IL-13, whereas treatment w

190 blet cell hyperplasia/hypertrophy, increased mucus production/secretion, and airway hyperreactivity.

191 suring lung inflammatory cells infiltration, mucus production, serum lgE levels, and alveolar macroph

192 bited airway inflammation, eosinophilia, and mucus production, significantly reduced Ag-specific IgE

193 ell as to the occurrence of wheezing, cough, mucus production, sinusitis, and acute bronchitis.

194 ction in both airway hyperresponsiveness and mucus production that corresponded to significant increa

195 sensitive to IL-13-induced GC metaplasia and mucus production through lower expression of IL-13Ralpha

196 balancing act between cell proliferation and mucus production to restore barrier integrity seems to d

197 ggravated airway inflammation, and increased mucus production together with pronounced airway hyperre

198 d IL-13, induce goblet cell hyperplasia with mucus production, ultimately resulting in worm expulsion

199 ces including airway hyperresponsiveness and mucus production via increased Th2 cytokines.

200 Mucus production was attenuated in lungs from HDM-treate

201 Furthermore, mucus production was decreased in FHL2-KO mice.

202 Mucus production was determined by means of periodic aci

203 es were noted, urinary calculi did not form, mucus production was normal, and renal function was pres

204 of Th1 cells on both airway eosinophilia and mucus production were abolished.

205 Changes in pulmonary mucus production were accompanied by an increase in pulm

206 Lung tissue inflammation and mucus production were assessed by means of flow cytometr

207 levels in broncho-alveolar lavage fluid, and mucus production were determined.

208 Lung inflammation and mucus production were increased in the airways of IL-12p

209 ibronchial and perivascular inflammation and mucus production were largely similar in both groups.

210 cally OVA-challenged mice, GC metaplasia and mucus production were observed in proximal but not in di

211 Importantly, airway hyperresponsiveness and mucus production were significantly reduced after treatm

212 thelial and subepithelial layers, as well as mucus production, were assessed in paraffin-embedded end

213 hils in the bronchoalveolar lavage fluid and mucus production, were assessed.

214 disease, specifically airway reactivity and mucus production, were increased in CCSP(-/-) mice after

215 airway eosinophilia and a marked increase in mucus production, while mice that received Th1 cells exh

216 d mechanical stress, inflammation, excessive mucus production with impaired mucociliary clearance, an

217 BL/6 mice that had low airway resistance and mucus production with little pulmonary inflammation.