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1 sing AlgB.D59N or H-AlgB delta1-145 remained mucoid.
2 lony morphology and phenotype referred to as mucoid.
3 s in cystic fibrosis patients are frequently mucoid.
4 ved on solid culture media is referred to as mucoid.
5 monas aeruginosa (PA) as either nonmucoid or mucoid.
6 se-negative lasB::Cm knock-out mutant in the mucoid 8821 background was constructed, and it showed a
9 s in Pseudomonas aeruginosa, are elevated in mucoid, alginate-producing bacteria and in response to i
14 To detect spontaneous mutations in csrRS, mucoid and large colony variants of M1 strain MGAS166 we
16 ate that elastase, when overproduced in both mucoid and non-mucoid cells, stimulates alginate synthes
18 imary clinical B. pseudomallei isolates with mucoid and nonmucoid colony morphologies from the same s
20 fibrosis pulmonary isolate FRD1, as well as mucoid and nonmucoid mutant strains, were monitored by A
21 s associated with ARF in the SLC region, 964 mucoid and nonmucoid pharyngeal isolates recovered in SL
22 t in addition to being intracellular in both mucoid and nonmucoid Pseudomonas aeruginosa, Ndk is also
23 found to promote phagocytic killing of both mucoid and nonmucoid strains as well as protection again
26 study, we observed that in CF isolates, the mucoid and the nonmotile phenotypes occur predominantly
27 robial susceptibilities of 48 CF strains (25 mucoid) and 50 non-CF strains to 12 anti-Pseudomonas age
30 ious reports of increased algR expression in mucoid backgrounds, and RpoS additionally plays a role i
35 bits and elicited opsonic antibodies against mucoid but not nonmucoid P. aeruginosa, but nonetheless
36 X-treated mice also had dramatically reduced mucoid cell hyperplasia, and airway responsiveness retur
38 -kDa Ndk-Scs complex specifically present in mucoid cell predominantly synthesizes GTP and UTP but no
39 omplex media but is greatly reduced when the mucoid cells are grown in mineral salts media or in pres
40 osa is greatly reduced in alginate-secreting mucoid cells isolated from the lungs of cystic fibrosis
42 22) P. aeruginosa strains were compared, the mucoid cells were cleared several-fold less efficiently
44 In contrast, Scnn1b-Tg mice infected with a mucoid CF isolate carried high bacterial burdens, produc
48 the secretion is triggered primarily in the mucoid CF isolate of strain 8821M (or in strain FRD1) bu
53 ariner transposon library using CF149, a non-mucoid clinical isolate with a misssense mutation in alg
54 r, the average amount of cyanide produced by mucoid clinical isolates was 4.7 +/- 0.85 micromol of HC
55 increase in bacterial hyaluronan production (mucoid colonies 200 mug per CFU and no detectable capsul
56 tified as csrR, caused the strain to produce mucoid colonies and to increase transcription of hasA, t
57 ive ("flesh-eating") infection often grow as mucoid colonies on primary culture but lose this colony
62 syrA was identified by its ability to confer mucoid colony morphology and by its ability to suppress
63 solates from these patients typically have a mucoid colony morphology due to overproduction of the ex
64 3 produced a transconjugant that exhibited a mucoid colony morphology, reflecting increased hyaluroni
66 The hldD, hldE, and waaF mutants exhibited a mucoid colony phenotype due to production of a colanic a
69 a usually undergoes a phenotypic switch to a mucoid colony, which is characterized by the overproduct
70 h cells from smooth-colony variants (SM) and mucoid-colony variants (MC) arising from phenotypic swit
75 omoter caused the overexpression of MucE and mucoid conversion in P. aeruginosa strains PAO1 and PA14
76 ion of the exopolysaccharide alginate causes mucoid conversion in Pseudomonas aeruginosa and is a poo
81 th cystic fibrosis are at increased risk for mucoid conversion of Pseudomonas aeruginosa, which contr
82 e C terminus of MucE (WVF) were required for mucoid conversion via two predicted proteases AlgW (DegS
83 Thus, even though dsbA is coregulated with mucoid conversion, it was not required for alginate prod
88 we tested wild-type strains PAO1, PA14, the mucoid cystic fibrosis isolate, FRD1 (mucA22+), and the
89 show here that a null mutation in kinB in a mucoid cystic fibrosis isolate, P. aeruginosa FRD1, did
90 structure of microvessel walls, formation of mucoid cysts initiated in the proximity of damaged micro
92 ar appearance, pronounced vacuolization, and mucoid degeneration, appearing as Wallerian degeneration
93 e found that P. aeruginosa strain PAO1 and a mucoid derivative of strain PAO1 each grew at dissolved
94 large fraction of P. aeruginosa CF isolates mucoid, did not abrogate AlgU-MucA interactions, althoug
95 iants of Cryptococcus neoformans (smooth and mucoid) differed in their abilities to promote increased
96 ns associated with cystic fibrosis are often mucoid due to the copious production of alginate, an exo
99 r (TNF)-alpha, a proinflammatory cytokine in mucoid effusion, markedly increased Muc2 mucin mRNA expr
102 than those involved in the production of the mucoid exopolysaccharide alginate, are turned on during
103 aboration of the extracellular, O-acetylated mucoid exopolysaccharide, or alginate, is a major microb
104 upon the conversion of P. aeruginosa to the mucoid, exopolysaccharide alginate-overproducing phenoty
106 Similar experiments were performed with mucoid films collected from the inferior conjunctival fo
111 he algT-mucABCD operon, MucD was detected in mucoid (FRD1) and nonmucoid (PAO1) parental strains and
113 ignal intensities and the so-called inverted mucoid impaction signal (IMIS) sign was qualitatively an
115 wild-type mice challenged with an LPS-rough mucoid isolate of P. aeruginosa lacking the CFTR ligand.
122 tro and were associated with selectivity for mucoid isolation, increased exacerbations, and mucoid co
123 y and proteomic analyses were performed on a mucoid kinB mutant and an isogenic nonmucoid kinB rpoN d
124 ction from laboratory isolates revealed that mucoid laboratory strains made sevenfold more HCN than t
125 gulated using isogenic S. aureus MN8 and MN8 mucoid (MN8m) strains, the latter of which constitutivel
126 atients with cystic fibrosis often display a mucoid morphology due to high levels of expression of th
127 re to estradiol, P. aeruginosa adopted early mucoid morphology, whereas short-term exposure inhibited
135 ts showed that ectopic expression of FleQ in mucoid, nonmotile CF isolates restored flagellum biosynt
136 that AlgT inhibits flagellum biosynthesis in mucoid, nonmotile P. aeruginosa cystic fibrosis isolates
140 ibits lawn bordering and roaming behavior on mucoid nonpathogenic bacteria and loss of pathogen avoid
141 charge was frequent or very frequent in 85%, mucoid or mucopurulent in 90%, and moderate to severe in
142 hose in desert tortoises and include serous, mucoid, or purulent discharge from the nares, excessive
145 tor was also associated with reduced odds of mucoid P. aeruginosa (OR, 0.77; P = .013) and Aspergillu
148 ntion of active elastase in the periplasm of mucoid P. aeruginosa and its role in the generation of t
149 sponse regulators activate alginate genes in mucoid P. aeruginosa appears not to be mediated by conve
151 it may play an important role in protecting mucoid P. aeruginosa biofilm bacteria from the human imm
152 ture and extracellular matrix composition of mucoid P. aeruginosa biofilms, through increased express
155 identified a protein(s), AlgZ, expressed in mucoid P. aeruginosa CF isolates that specifically bound
156 The calcium-induced extracellular matrix of mucoid P. aeruginosa consists primarily of the virulence
158 investigated mechanisms of the emergence of mucoid P. aeruginosa in CF by analyzing the status of mu
162 ung infections could not be established with mucoid P. aeruginosa in either cystic fibrosis or wild-t
163 fection, chronic P. aeruginosa infection and mucoid P. aeruginosa in individuals with cystic fibrosis
165 Indeed, chronic infection of the lung by mucoid P. aeruginosa is a major cause of morbidity and m
167 hesis by laboratory and clinical isolates of mucoid P. aeruginosa is necessary and sufficient to atte
168 airway epithelia to the stimuli presented by mucoid P. aeruginosa is not proinflammatory and, hence,
173 rogated AIgU-dependent rpoH transcription in mucoid P. aeruginosa laboratory isolates and CF isolates
175 in CF is the result of a global induction in mucoid P. aeruginosa of lipoproteins that act as proinfl
177 Transcriptional profiling analyses comparing mucoid P. aeruginosa strains to their isogenic algR dele
180 tion of alginate maximizes the resistance of mucoid P. aeruginosa to antibody-independent opsonic kil
181 te plays an important role in the ability of mucoid P. aeruginosa to form biofilms and to resist comp
182 is the molecular basis for the resistance of mucoid P. aeruginosa to normally nonopsonic but alginate
183 ds or beads containing a clinical isolate of mucoid P. aeruginosa were instilled in the right lung of
191 isk factors, only respiratory infection with mucoid PA correlated significantly with bronchiectasis (
192 isolates were more likely to be infected by mucoid PA, and they showed a narrow T-cell epitope respo
193 cantly related to respiratory infection with mucoid PA; attempts to prevent bronchiectasis should inc
195 Overexpression of algW in PAO1 resulted in a mucoid phenotype and alginate production, even in the ab
196 tion of phpA was found to correlate with the mucoid phenotype and an increase in algD transcription i
197 system that, when inactivated, results in a mucoid phenotype and enhanced virulence in mouse infecti
198 biofilms and the selection of mutants with a mucoid phenotype are major adaptations that allow its pe
199 conversion of Pseudomonas aeruginosa to the mucoid phenotype coincides with the establishment of chr
200 ion of invasive virulence factors and have a mucoid phenotype due to the production of an alginate ca
204 well-studied mechanism for transition to the mucoid phenotype is mutation of mucA, leading to loss of
205 regulator of both sigma(22) activity and the mucoid phenotype is the cognate anti-sigma factor MucA.
206 we demonstrated that in vivo switching to a mucoid phenotype occurred in two mice strains and was as
208 Conversion of Pseudomonas aeruginosa to the mucoid phenotype plays a major role in the pathogenesis
211 rity, and in the concomitant appearance of a mucoid phenotype that is reminiscent of cells in the ear
214 The algXDelta::Gm mutant was restored to the mucoid phenotype with wild-type P. aeruginosa algX provi
216 riant was experimentally proven to cause the mucoid phenotype, and corresponding resistance to phagoc
229 [FEV(1)]) of the CFTR gene genotype, gender, mucoid Pseudomonas aeruginosa (MPA) infection status, pr
233 fficacy of azithromycin in a murine model of mucoid Pseudomonas aeruginosa endobronchial infection.
234 maintenance of chronic lung infections with mucoid Pseudomonas aeruginosa in patients with cystic fi
235 The exopolysaccharide alginate, produced by mucoid Pseudomonas aeruginosa in the lungs of cystic fib
236 tible to chronic pulmonary disease caused by mucoid Pseudomonas aeruginosa strains that overproduce t
240 tors in nontypeable, alginate overproducing (mucoid) Pseudomonas aeruginosa strains isolated from cys
241 we screened a transposon library in the non-mucoid reference strain PAO1, and identified a mutant th
242 were found to display phenotypes which were mucoid relative to the phenotype of the parental algB st
244 hrough viscoelastic cervical mucus and other mucoid secretions to reach the site of fertilization.
245 By using a representative strain of the mucoid serotype 3 clone, rough phase variants with a div
246 ations were found to be strain specific: the mucoid strain 18A experienced mutations in alginate prod
250 gG activity, a mutant was constructed in the mucoid strain FRD1 with a defined non-polar deletion of
252 on the eradication of biofilms formed by the mucoid strain of Pseudomonas aeruginosa and investigated
253 FU of group B streptococci or 10(7) CFU of a mucoid strain of Pseudomonas aeruginosa by intratracheal
255 eatment with S-nitrosoglutathione, while the mucoid strain PAO578II showed no further upregulation ab
256 pted agar bead murine model using a clinical mucoid strain that demonstrates the key features of tran
260 tions are cleared but chronic infection with mucoid strains ensues in the majority of CF patients and
265 an extracellular polysaccharide produced by mucoid strains of Pseudomonas aeruginosa that are typica
267 on resulted in suppression of mucoidy in all mucoid strains tested, indicating that sigma factor comp
269 l), is required for biofilm formation in non-mucoid strains that do not rely on alginate as the princ
270 uggests that the reduced CBC observed in the mucoid strains was due to masking of the collagen adhesi
271 ) of nonmucoid strains and 40% (24 of 60) of mucoid strains were definitively identified as Pseudomon
272 n were non-CF strains (P < 0.0001), although mucoid strains were not more likely to have serious disc
278 MAb-reactive (nonmucoid) and nonreactive (mucoid) strains from the same patient exhibited identica
284 und to be downregulated in the hypervirulent mucoid switch variant, both during logarithmic growth an
285 mimicked the hypervirulent phenotype of the mucoid switch variant, which is characterized by decreas
286 hese mutants ranged from being only slightly mucoid to being indistinguishable from that of the origi
288 erotype 19 gives rise to variants (the small mucoid variant [SMV] and the acapsular small-colony vari
292 cerebrospinal fluid (CSF) fungal burden for mucoid variant-infected rats, although brain fungal burd