ライフサイエンスコーパス: mucus production

1 locking the chemokines also decreased airway mucus production.

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

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

4 results from significant decreases in airway mucus production.

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

6 by significant increases in inflammation and mucus production.

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

8 cialized and nonredundant role in intestinal mucus production.

9 e revealed no enhancement of inflammation or mucus production.

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

11 he accumulation of eosinophils and augmented mucus production.

12 lar epithelial cells staining positively for mucus production.

13 orrelated with reduction in allergen-induced mucus production.

14 production, airway hyperresponsiveness, and mucus production.

15 y completely protected from allergen-induced mucus production.

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

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

18 deling, including peribronchial fibrosis and mucus production.

19 rance occurred that was potentially aided by mucus production.

20 ntagonist, prevented airway eosinophilia and mucus production.

21 tributes to the severity of inflammation and mucus production.

22 way responsiveness, tissue eosinophilia, and mucus production.

23 educed airway eosinophilia without affecting mucus production.

24 pletely abolished both lung inflammation and mucus production.

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

26 airways were epithelial cell hypertrophy and mucus production.

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

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

29 tically important in Th2 cell stimulation of mucus production.

30 of asthma, including airway eosinophilia and mucus production.

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

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

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

34 sed by airway remodelling, inflammation, and mucus production.

35 rway epithelium to study Tmem16a function in mucus production.

36 eins such as ZO-1 and occludin, and elevated mucus production.

37 duction, enhanced eosinophilia, and elevated mucus production.

38 production, airway hyper-responsiveness and mucus production.

39 e magnitude of the inflammatory response and mucus production.

40 ociated FOXP3 gene expression, and increased mucus production.

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

42 ioalveolar lavage fluid, and enhanced airway mucus production.

43 eosinophils and lymphocytes, and aggravated mucus production.

44 onchiolar inflammation, and increased airway mucus production.

45 hey regulate goblet cell differentiation and mucus production.

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

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

48 nflammation, airway hyperresponsiveness, and mucus production.

49 known to induce eosinophil accumulation and mucus production.

50 overexpression of memIL-13Ralpha2 increased mucus production.

51 airway inflammation in these diseases affect mucus production?

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

53 e in experimental asthma with reduced airway mucus production, airway hyperresponsiveness and eosinop

54 Mucus production, airway hyperresponsiveness to methacho

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

56 rk of allergic asthma and is associated with mucus production, airway hyperresponsiveness, and shortn

57 7A had augmented airway hyperresponsiveness, mucus production, airway inflammation, and IL-13-induced

58 the importance of targeting the epithelium, mucus production, airway smooth muscle, and small airway

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

60 ction compared with wild-type mice; however, mucus production and airway hyperreactivity were not aff

61 flammation, cytokine expression and release, mucus production and airway hyperresponsiveness were mea

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

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

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

65 et cell metaplasia, accompanied by increased mucus production and airway secretions.

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

67 transcriptome-wide association analyses for mucus production and chronic cough also identified MUC5A

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

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

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

71 Warmer SST was also accompanied by decreased mucus production and decreased Symbiodiniaceae abundance

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

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

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

75 Mucus production and epithelial integrity was assessed i

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

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

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

79 Likewise, FR inhibits mucus production and secretion in air-liquid interface c

80 dy elimination, as well as the initiation of mucus production and secretion.

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

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

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

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

85 a local mucosal defect in type 2 cytokines, mucus production, and a selective local immunoglobulin A

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

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

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

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

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

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

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

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

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

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

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

97 pe 2 immunity and eosinophilic inflammation, mucus production, and bronchial hyperreactivity in respo

98 ion of epithelial-epidermal differentiation, mucus production, and cellular adhesion were associated

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

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

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

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

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

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

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

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

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

108 inophilia, airway hyperresponsiveness (AHR), mucus production, and IgE levels.

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

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

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

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

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

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

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

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

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

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

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

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

121 e enteral side fuels goblet cells to support mucus production, and the serosal side loosens the epith

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

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

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

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

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

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

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

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

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

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

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

133 Excessive mucus production by airway epithelium is a major charact

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

135 Mucus production by goblet cells of the large intestine

136 blocking antibodies and strong reduction of mucus production by goblet cells.

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

138 We tested the hypothesis that (1) mucus production can be included in the cell response to

139 We conclude that mucus production can be involved in the response to a fu

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

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

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

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

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

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

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

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

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

149 dust mite (HDM) challenge with decreases in mucus production, cytokine secretion, and collagen depos

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

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

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

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

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

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

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

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

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

159 ent parenchymal immune cell infiltration and mucus production for at least 7 wk postinfection.

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

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

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

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

164 y model and increased airways resistance and mucus production in a house dust mite (HDM) asthma model

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

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

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

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

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

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

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

172 rway pathology, down-regulation of ILC2s and mucus production in asthma.

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

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

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

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

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

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

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

180 let cells to regulate epithelial renewal and mucus production in mice and humans, but its function in

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

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

183 n reducing IgE levels, AHR, eosinophilia and mucus production in mouse models of asthma analyzed up t

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

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

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

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

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

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

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

191 tivation, ROS production, NET formation, and mucus production in the airways.

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

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

194 osure diminished goblet cell hypertrophy and mucus production in the lung in response to airway infec

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

196 eration, the percentages of eosinophils, and mucus production in the lung.

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

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

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

200 in-2 expression, IL-4/IL-5/IL-13 production, mucus production) in the airways and lungs was significa

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

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

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

204 ith these observations, microRNAs regulating mucus production, inflammation, Th2 effector functions,

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

206 Type-2 cytokines promote mucus production, innate immune cell recruitment, and sm

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

208 Increased mucus production is a critical factor impairing lung fun

209 Excessive mucus production is an important pathological feature of

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

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

212 Given that anticholinergics only decrease mucus production, it is unknown whether prophylactic app

213 Consequently, virus infection alters mucus production, leading to an increase in mucus-associ

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

215 promotes secretory cell differentiation and mucus production; levels of IDO1 are positively correlat

216 red to be unaffected by both stressors, with mucus production maintaining microbial community composi

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

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

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

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

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

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

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

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

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

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

227 nhibition, co-aggregation ability, enhancing mucus production, production of bacteriocins, and modula

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

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

230 ring neonatal murine RSV infection decreased mucus production, reduced cellular infiltrates to the lu

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

232 acterized by productive cough with excessive mucus production, resulting in quality-of-life impairmen

233 cellular proliferation and differentiation (mucus production, secretin receptor expression, and prim

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

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

236 symptoms including, persistent coughing and mucus production, shortness of breath, wheezing, and che

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

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

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

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

241 increasing cytokine/chemokine expression and mucus production, thus demonstrating redundant functions

242 -parasite type 2 immune responses that drive mucus production, tissue remodeling and immune cell infi

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

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

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

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

247 Mucus production was attenuated in lungs from HDM-treate

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

249 Mucus production was determined by means of periodic aci

250 In both parts, mucus production was more than 70% lower in each EDP-938

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

252 Mucus production was similar in both treatment groups.

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

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

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

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

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

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

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

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

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

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

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

264 ay remodeling via STAT3-mediated increase in mucus production, which provide new insight in our under

265 s in mucus-producing goblet cells to enhance mucus production, which shapes the gut microbial communi

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

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

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