ライフサイエンスコーパス: mucus

1 of the cornea and conjunctiva, and amount of mucus.

2 ecretes large quantities of a matrix such as mucus.

3 over the range that is characteristic of CF mucus.

4 ZG16 hindered bacterial penetration into the mucus.

5 ar processing of MUC2 to generate protective mucus.

6 loss after repeated submersions in blood and mucus.

7 natural environment in soils, sediments, or mucus.

8 the role of Pil3 pilus in binding to colonic mucus.

9 lls and prevents viruses becoming trapped in mucus.

10 lls and prevents viruses becoming trapped in mucus.

11 chor highly diverse commensal communities to mucus.

12 he cilia using glucose internalized from the mucus.

13 on a dynamic interaction between intestinal mucus, a bacterial toxin, and a toxin regulatory system.

14 To further investigate mucus abnormalities, here we studied airway surface liqu

15 d pro-fibrotic signaling, and also prevented mucus accumulation and development of AHR in mice.

16 owing bacterial infection, inflammation, and mucus accumulation to progressively destroy the lungs.

17 ow rate and buffering capacity and increased mucus acidity.

18 ct evidence for a CBM40 as a novel bacterial mucus adhesin.

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

20 mate Zg16(+/+) The more penetrable Zg16(-/-) mucus allowed Gram-positive bacteria to translocate to s

21 VCBPs and bacteria colocalize to chitin-rich mucus along the intestinal wall.

22 osinophils in the peripheral blood and stool mucus and allergen-specific lymphocyte stimulation test.

23 note that almost all biological fluids (e.g. mucus and blood) are viscoelastic in nature, and this fi

24 extremely adhesive biological fluids such as mucus and blood.

25 the majority of tSC is in free form in trout mucus and free tSC is able to directly bind bacteria.

26 an LS174T goblet-like cells were depleted of mucus and had elevated levels of MUC2 mRNA expression af

27 zes the current understanding of respiratory mucus and its interactions with the respiratory pathogen

28 either glpG or glpR impaired ExPEC growth in mucus and on plates containing the long-chain fatty acid

29 and must swim through viscoelastic cervical mucus and other mucoid secretions to reach the site of f

30 lung IL-13 protein levels, decreased airway mucus and reactivity, attenuated weight loss, and simila

31 We examined the functional potential of mucus and stool microbial communities in the mdr1a (-/-)

32 o-rheology experimental data on cell culture mucus, and a numerical algorithm is developed for the cu

33 ns exposed to G. duodenalis were depleted of mucus, and in vivo mice infected with G. duodenalis had

34 There are numerous proteins in the nasal mucus, and they contribute to olfaction through various

35 These findings highlight the role of mucus as a responsive biomaterial, and reveal a mechanis

36 ructural rearrangements of the components of mucus as well as biochemical modifications to their adhe

37 his occurs because antibiotics reinforce the mucus barrier by eliminating sulfide-producing bacteria

38 is as part of C12-HSL's effect on intestinal mucus barrier function.

39 this region of the GI tract, the protective mucus barrier is poorly developed but matures to full th

40 cular formulation's ability to penetrate the mucus barrier passively.

41 e same niche, may affect the capacity of the mucus barrier to retain commensal E. coli.

42 biotic represents a strategy to overcome the mucus barrier, increase local drug concentrations, avoid

43 y fiber, the gut microbiota, and the colonic mucus barrier, which serves as a primary defense against

44 nt source, leading to erosion of the colonic mucus barrier.

45 in the reported subdiffusion of particles in mucus, based on the measured mean squared displacements

46 f drug carriers with enhanced penetration of mucus, brain tissues and other extracellular matrices.

47 le genes that contribute to ExPEC fitness in mucus broth were identified, with genes that are directl

48 s, pH1N1low-1 was significantly inhibited by mucus but pH1N1-1 was not.

49 vivo that CotE enables binding of spores to mucus by direct interaction with mucin and contributes t

50 We sought to determine the role of impaired mucus clearance in the pathogenesis of allergen-induced

51 cal significance is expected to be increased mucus clearance rates in cholinergically stimulated airw

52 ride, improving airway surface hydration and mucus clearance, reduced allergen-induced inflammation i

53 mucus partial osmotic pressures, and reduced mucus clearance.

54 ed the effects of therapeutic improvement of mucus clearance.

55 showed bacteria with higher motility in the mucus close to the host epithelium compared with cohouse

56 In vitro, tSC present in mucus coats trout commensal isolates such as Microbacter

57 (zymogen granulae protein 16) as an abundant mucus component.

58 ensitive to the biochemical modifications of mucus components exhibited significantly different trans

59 factors, including the innate immune system, mucus composition, and diet, have been identified as det

60 Purpose To assess the diagnostic accuracy of mucus contrast characterization by using magnetic resona

61 rs to induce characteristic modifications of mucus contrasts that are assessable by using a noninvasi

62 They find that a fiber-free diet promotes mucus-degrading bacteria and susceptibility to Citrobact

63 ributes to reduced airway hydration, causing mucus dehydration, decreased mucociliary clearance, and

64 Absence of mucus deposition inside the bronchiole wall and low coll

65 ry neurons chemosensory cilia are elongated, mucus embedded, fully exposed structures particularly am

66 mucus layer and their numbers controlled by mucus-embedded antimicrobial peptides, preventing invasi

67 IgM from clonally affiliated PCs, recognized mucus-embedded commensals.

68 deprivation, together with a fiber-deprived, mucus-eroding microbiota, promotes greater epithelial ac

69 ymers dramatically compressed murine colonic mucus ex vivo and in vivo.

70 primary macromolecular components of airway mucus, facilitate airway clearance by mucociliary transp

71 er 2 consecutive weeks and sampled cutaneous mucus, feces and water at 0, 7 &14 days.

72 Levels of airway inflammation, mucus, fibrosis, and airway smooth muscle were no differ

73 in enabling it to traverse and colonize the mucus-filled intestinal crypts of their host, a necessar

74 concentration dropped at the surface of the mucus flow is simulated as a function of Peclet number.

75 recently utilized for an in situ study of CF mucus formed by airway cell cultures.

76 by the coral and/or dissolution of DMS-rich mucus formed by the coral during air exposure.

77 The blue glow of the mucus from Chaetopterus involves a photoprotein, iron an

78 icantly different transport profiles through mucus from high- and low-risk patients.

79 on, we assessed the permeability of cervical mucus from non-pregnant ovulating (n = 20) and high- (n

80 tively charged, carboxylated microspheres in mucus from pregnant patients was significantly restricte

81 ivery of drugs that improve the clearance of mucus from the lungs and treat the consequent infection,

82 as related to tethering of MUC5AC-containing mucus gel domains to mucus-producing cells in the epithe

83 ted the nanoporous and highly adhesive human mucus gel layer that constitutes a primary barrier to re

84 ns MUC5AC and MUC5B are organized within the mucus gel or how this gel contributes to airway obstruct

85 thma, induced the formation of heterogeneous mucus gels and dramatically impaired mucociliary transpo

86 with reticular basement membrane thickness, mucus gland area, collagen area, and submucosal effector

87 We discuss molecules-mucus glycans and IgA-that affect microbe adhesion and i

88 the gut microbiota resorts to host-secreted mucus glycoproteins as a nutrient source, leading to ero

89 We previously showed differences in mucus gut microbiota composition preceded colitis-induce

90 Respiratory mucus has numerous functions and interactions, both with

91 Proteomic analyses of mucus have identified the lectin-like protein ZG16 (zymo

92 ents focusing on virions or nanoparticles in mucus have measured mean-square displacements and report

93 The rheological properties of intestinal mucus have therefore been the subject of many investigat

94 strate that gut polymers do in fact regulate mucus hydrogel structure, and that polymer-mucus interac

95 yet whether such polymers interact with the mucus hydrogel, and if so, how, remains unclear.

96 from germ-free mice strongly compressed the mucus hydrogel, whereas exposure to luminal fluid from s

97 he major structural components of protective mucus hydrogels on mucosal surfaces are the secreted pol

98 gs, particularly neutrophils and mast cells, mucus hyper-production and airway thickening) in an expe

99 Studies were performed to test whether mucus hyperconcentration and increased partial osmotic p

100 d the hypothesis that CB is characterized by mucus hyperconcentration, increased mucus partial osmoti

101 atures including airway hyperresponsiveness, mucus hyperplasia, airway eosinophilia, and type 2 pulmo

102 duce features of RSV lung disease, including mucus hyperplasia, in murine lungs and that HIS mice can

103 Chronic mucus hypersecretion (CMH) is common among smokers and i

104 irway disease characterized by inflammation, mucus hypersecretion and abnormal airway smooth muscle (

105 chronic airway inflammation, which leads to mucus hypersecretion and airway hyperresponsiveness.

106 strate that Lyn overexpression decreased the mucus hypersecretion and levels of the muc5ac transcript

107 d that Lyn overexpression ameliorated airway mucus hypersecretion by down-regulating STAT6 and its bi

108 tive Rho-A/Rho kinase inhibitor, affects the mucus hypersecretion by suppressing MUC5AC via signal tr

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

110 nhibitor NU7441 reduced airway eosinophilia, mucus hypersecretion, airway hyperresponsiveness, and OV

111 eactivity, eosinophilic airway inflammation, mucus hypersecretion, and Ag-specific Ig production.

112 sease that is characterized by inflammation, mucus hypersecretion, and airway hyperresponsiveness.

113 airway hyperresponsiveness, gene expression, mucus hypersecretion, and airway inflammation was assess

114 lar infiltration with concomitant epithelial mucus hypersecretion, goblet cell metaplasia, subepithel

115 onses and increases viral titres, leading to mucus hypersecretion.

116 esulting in increased airway eosinophils and mucus hypersecretion.

117 ne19F induces relatively high viral load and mucus in mice.

118 lood in stool (11.8% vs 29.6%; P < .001), or mucus in stool (2.1% vs 5.6%; P = .048) but more likely

119 In the mouse colorectum, MPP penetrated into mucus in the deeply in-folded surfaces to evenly coat th

120 s the formation of protein plugs and viscous mucus in the ducts, which could otherwise lead to pancre

121 The main structural component of the mucus in the gastrointestinal tract is the MUC2 mucin.

122 ts inability to penetrate the thick DNA-rich mucus in the lungs of these patients, leading to low ant

123 ment in individual VAS symptoms (rhinorrhea, mucus in throat, nasal blockage, and sense of smell), pa

124 This suggests that phage adherence to mucus increases encounters with bacterial hosts by some

125 th ferric and ferrous iron were found in the mucus, indicating the occurrence of both oxidase and red

126 e mucus hydrogel structure, and that polymer-mucus interactions can be described using a thermodynami

127 ration in shear leading to a peak in the air-mucus interface at the middle of the culture and a depre

128 nt of flow profiles and the shape of the air-mucus interface.

129 Colonic mucus is a key biological hydrogel that protects the gut

130 Hypersecretion of mucus is an important component of airway remodeling and

131 multi-mode nonlinear constitutive model for mucus is constructed directly from micro- and macro-rheo

132 inding of R. gnavus ATCC 29149 to intestinal mucus is sialic acid mediated.

133 ia and bacterial components can traverse the mucus layer and contact host cells.

134 tly improved permeability through intestinal mucus layer and epithelia.

135 underscored by decreased thickness of the OE mucus layer and increased numbers of immune cells within

136 ta, Proteobacteria were present in the inner mucus layer and invaded mucosal tissues.

137 a are physically separated from villi by the mucus layer and their numbers controlled by mucus-embedd

138 ound in mucin, a component of the intestinal mucus layer and thus one of the prime adherence targets

139 achieved in part by the presence of a dense mucus layer at the epithelial surface and by the product

140 r less than 40 nm are able to pass through a mucus layer by passive Brownian motion.

141 The mucus layer coating the airways is constantly moved alon

142 The mucus layer coating the pulmonary airways is moved along

143 A mucus layer coats the gastrointestinal tract and serves

144 rticularly true when pathogens encounter the mucus layer covering the respiratory tract.

145 The potential positive role of the mucus layer for cellular uptake and the fate of the colo

146 cells were mostly trapped within the surface mucus layer in WT mice.

147 The gastrointestinal mucus layer is colonized by a dense community of microbe

148 The mucus layer is critical in limiting contact between host

149 s comprehensive insight into the dynamics of mucus layer maturation upon bacterial colonization of ge

150 of functions in pathogen resistance such as mucus layer modifications and hydration, tight junction

151 The mucus layer provides an essential first host barrier to

152 something that is achieved by a dense inner mucus layer that lines the epithelial cells.

153 an inability to pass through the intestinal mucus layer to directly contact the epithelium.

154 Zg16(-/-) mice have a distal colon mucus layer with normal thickness, but with bacteria clo

155 robial peptide production, maturation of the mucus layer, and improved barrier function.

156 disease (IBD) are associated with a reduced mucus layer, potentially leading to dysbiosis associated

157 s (IEC-Cosmc(-/y)) resulted in a compromised mucus layer, spontaneous microbe-dependent inflammation,

158 tract are in intimate contact with the outer mucus layer.

159 at are secreted by epithelial cells into the mucus layer.

160 dvantage for penetrating the viscous stomach mucus layer.

161 mum, devoid of inner membranes embedded in a mucus layer.

162 tes enhanced the retention in the intestinal mucus layer.

163 lls and abundantly secreted into the surface mucus layer.

164 how that the interaction between viruses and mucus may be an important factor in viral transmissibili

165 ally a commensal colonizer of human skin and mucus membranes, but, due to its ability to form biofilm

166 responsiveness (AHR), lung inflammation, and mucus metaplasia in a dual Th2/Th17 model of asthma.

167 it only partially mediates inflammation and mucus metaplasia in a mixed Th2/Th17 model of steroid-re

168 These data suggest that IL-13 drives AHR and mucus metaplasia in a STAT6-dependent manner, without di

169 hilia and neutrophilia, tissue inflammation, mucus metaplasia, and AHR that were partially reversible

170 with IL-17A significantly attenuated AHR and mucus metaplasia.

171 13, IL-17, eotaxin, and eosinophils and more mucus metaplasia.

172 Whereas the FA-Tg(+) mice exhibited marked mucus obstruction and Th2 responses, SHS-Tg(+) mice disp

173 d airway neutrophilia and reduced mortality, mucus obstruction, and emphysema in Scnn1b-Tg mice.

174 Addition to the mucus of elements with inhibitory/potentiary effect on f

175 protein (Sandercyanin)-ligand complex in the mucus of walleyes.

176 The inner colon mucus of Zg16(-/-) animals had a higher load of Gram-pos

177 affinities of strains for substrates such as mucus or food particles, combined with more rapid replic

178 ays (e.g., inflammatory mediators, excessive mucus) or an altered neuronal phenotype is unknown.

179 es clearance, and the increased transport of mucus out of the airways restores ASL depth while cleans

180 rotrophin 4 (NT4) plays an essential role in mucus overproduction after early life allergen exposure

181 -) mice were protected from allergen-induced mucus overproduction and changes along the nerve-PNEC ax

182 rway goblet cell differentiation and related mucus overproduction are critical processes in the devel

183 C axis may be a valid treatment strategy for mucus overproduction in airway diseases, such as childho

184 Last, GABA installation restored mucus overproduction in NT4(-/-) mice after early life a

185 Early life allergen-induced mucus overproduction requires augmented neural stimulati

186 cell differentiation with a 75% reduction in mucus overproduction while improving airway responsivene

187 granulocytosis, airway hyperresponsiveness, mucus overproduction, collagen deposition, and Th2/Th17

188 rized by mucus hyperconcentration, increased mucus partial osmotic pressures, and reduced mucus clear

189 y and uniformly transported non-mucoadhesive mucus-penetrating particles (MPP) to epithelial surfaces

190 likely responsible for massive alteration in mucus phenotype.

191 l regeneration line, Acanthamoeba keratitis, mucus plaque keratopathy, medication-related keratopathy

192 ter the overall permeability of the cervical mucus plug, our findings suggest that the latter mechani

193 al ascension across a dysfunctional cervical mucus plug.

194 of disease heterogeneity, including regional mucus plugging associated with abnormal lung perfusion i

195 tasis and likely represents a major cause of mucus plugging in asthma.

196 t represent a protective strategy to prevent mucus plugging of distal airways and thus impaired venti

197 ll as MRI-defined airway wall abnormalities, mucus plugging, and abnormal lung perfusion in infants a

198 goblet cell hyperplasia; hyper IgE syndrome; mucus plugging; and extensive inducible BALT.

199 of airway remodeling and contributes to the mucus plugs and airflow obstruction associated with seve

200 Here, we demonstrated that mucus plugs from individuals with fatal asthma are heter

201 RgCBM40 binds to mucus produced by goblet cells and to purified mucins, p

202 ng of MUC5AC-containing mucus gel domains to mucus-producing cells in the epithelium.

203 gallolyticus strain UCN34, adhered better to mucus-producing cells such as HT-29-MTX than to the pare

204 Furthermore, the numbers of mucus-producing goblet cells and inflammatory cell infil

205 le to reduce the adhesion of C. difficile to mucus-producing intestinal cells.

206 adhered to mucin glycoproteins and protected mucus-producing tissue culture cells in vitro.

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

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

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

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

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

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

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

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

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

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

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

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

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

220 7A had augmented airway hyperresponsiveness, mucus production, airway inflammation, and IL-13-induced

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

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

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

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

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

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

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

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

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

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

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

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

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

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

235 ociated FOXP3 gene expression, and increased mucus production.

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

237 ioalveolar lavage fluid, and enhanced airway mucus production.

238 eosinophils and lymphocytes, and aggravated mucus production.

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

240 rance occurred that was potentially aided by mucus production.

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

242 In cystic fibrosis (CF) altered mucus properties impair mucociliary transport.

243 , we show that subdiffusion in normal acidic mucus provides a more effective barrier against infectio

244 etermining the viscoelastic properties of CF mucus, providing an improved understanding of this disea

245 he airway lumen might include binding to the mucus, reduced uptake by respiratory cells and reduced t

246 The damaged epithelium impairs mucus removal and facilitates bacterial infection with i

247 current findings we propose that respiratory mucus represents an understudied host-restriction factor

248 eplacement of tethered mucus with untethered mucus restored mucociliary transport.

249 nsive biomaterial, and reveal a mechanism of mucus restructuring that must be integrated into the des

250 Functional failure of CFTR results in mucus retention and chronic infection and subsequently i

251 ercyanin-BLA complex, purified from the fish mucus, reveals a glycosylated protein with a lipocalin f

252 This study investigates the roles that mucus rheology, wall effects, and HBE culture geometry p

253 Weekly nasal mucus samples were analyzed for RVs, and respiratory sym

254 asitize the surface of the fish, feeding off mucus, scales and underlying tissue.

255 ult from an increase in the viscosity of the mucus secreted by epithelial cells that line the airways

256 significant difference in the viscosities of mucus secreted by normal and CF human airway cell cultur

257 ressing tissue eosinophils and inflammation, mucus-secreting cell (MSC) numbers, type 2-associated cy

258 tissue physiology, including hyperplasia of mucus-secreting goblet cells and smooth muscle hypercont

259 eosinophilia, type 2 cytokine production and mucus secretion after allergen inhalation.

260 ole in murine asthma, mediating both AHR and mucus secretion after HDM exposure.

261 rine lactone (C4-HSL), on cell viability and mucus secretion in LS174T cells.

262 cant depletion of goblet cell metaplasia and mucus secretion markers after HDM exposure.

263 y shown to regulate airway cell cytokine and mucus secretion, and transepithelial Cl(-) current.

264 eatment of disorders of epithelial fluid and mucus secretion, hypertension, asthma, and possibly canc

265 inistration to the lung resulted in enhanced mucus secretion, inflammatory cell recruitment, and cyto

266 hma is characterized by airway inflammation, mucus secretion, remodeling and hyperresponsiveness (AHR

267 es were assessed for airway inflammation and mucus secretion.

268 pe and luxO mutant grown in mouse intestinal mucus showed that 60% of the genes that were downregulat

269 recovery after photobleaching in respiratory mucus showed that mechanisms involved in the prolonged p

270 ks the nutritive potential of 9-O-acetylated mucus sialic acids for foraging by bacteria that otherwi

271 One of the identified mucus-specific fitness genes encodes the rhomboid protea

272 ot; this suggests that gut microbes modulate mucus structure by degrading polymers.

273 e been identified as potential regulators of mucus structure, the polymeric composition of the gut en

274 e, we used gentle centrifugation to obtain a mucus supernatant showing no inhibition to oxidizers, al

275 n effective escape from epithelial cells and mucus that are shed into the acidic bactericidal lumen a

276 ized by the accumulation of sticky and heavy mucus that can damage several organs.

277 he GI tract, including wide variation in pH, mucus that varies in thickness and structure, numerous c

278 in healthy carriers is maintained by colonic mucus, the major constituent of which is the glycoprotei

279 nic mice, mucus transport in these mice, and mucus transport in a sheep model of CF.

280 othesized to be a key variable that controls mucus transport in healthy persons versus cessation of t

281 s, from arterial blood vessels and bronchial mucus transport in humans to bacterial flow through poro

282 SPX-101 increased mucus transport in the beta-ENaC mouse model as well as

283 ed by survival of beta-ENaC-transgenic mice, mucus transport in these mice, and mucus transport in a

284 dition, sputum partial osmotic pressures and mucus transport rates were measured in subjects with CB.

285 tion, leading to significant improvements in mucus transport.

286 Abnormalities of mucus viscosity play a critical role in the pathogenesis

287 pharmacologic therapies aimed at decreasing mucus viscosity.

288 athogen residing in the oxidant-rich gastric mucus was studied.

289 When the olfactory mucus was washed out by the injection of PBS to mouse na

290 We measured millimolar glucose in rat mucus; we detected glucose transporter GLUT3 in rat and

291 for symptom score (P<0.05), and the AUC for mucus weight were lower in all groups receiving ALS-0081

292 IgT titers are confined to the gill and skin mucus, whereas F. major-specific IgM titers are only det

293 e particles displayed subdiffusive motion in mucus, whereas T4hoc particles displayed normal diffusio

294 characterize the viscoelastic properties of mucus, which enables simultaneous measurement of rheolog

295 The development of pathologic mucus, which is not readily cleared from the airways, is

296 that are important for growth in intestinal mucus, which is thought to be a major source of nutrient

297 Our previous studies revealed that mucus with abnormal behavior impaired mucociliary transp

298 The presence of mucus with both high T1 and low T2 signal intensities an

299 Replacement of tethered mucus with untethered mucus restored mucociliary transpo

300 By concentrating phages in an optimal mucus zone, subdiffusion increases their host encounters