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1 B. fragilis 9343 expresses at least three capsular polys
2 B. fragilis enterotoxin did not affect enterocyte viabil
3 B. fragilis enterotoxin was associated with HT-29 cell r
4 B. fragilis lacking PSA is unable to restrain T helper 1
5 B. fragilis OxyR and Dps proteins showed high identity t
6 B. fragilis was anergistic (antagonistic) to E. coli in
7 B. fragilis, as well as purified capsular polysaccharide
8 B. fragilis, which by itself is immunogenic, did not pro
9 97.3%) Actinomyces strains, 42 of 46 (91.3%) B. fragilis group strains, 79 of 103 (76.7%) Clostridium
11 analysis of the PS A biosynthesis loci of 50 B. fragilis isolates indicates that regions flanking eac
14 mylase indicates that amino acid residue 90 (B. fragilis numbering) plays an important role in confer
15 ributes to sepsis in mice, and we identify a B. fragilis protease called fragipain (Fpn) that is requ
17 NAc as the sole carbon source, we isolated a B. fragilis mutant strain that can grow on this substrat
21 a scan of the Flavobacterium johnsoniae and B. fragilis genomes for putative promoters, resulting in
23 ay an altered serum metabolomic profile, and B. fragilis modulates levels of several metabolites.
26 aling that Tn5520 mobilizes plasmids in both B. fragilis and Escherichia coli at high frequency and a
27 ction or commensalism, induction of IL-10 by B. fragilis is critical to this microbe's interactions w
28 Whether the virulence mechanisms employed by B. fragilis during infections differ from those employed
29 zation of the gnotobiotic mouse intestine by B. fragilis requires that the organism synthesize only a
30 ite that is increased by MIA and restored by B. fragilis causes certain behavioral abnormalities, sug
32 ize microbial biogeography within the colon, B. fragilis penetrates the colonic mucus and resides dee
33 nted indicate that during aerobic conditions B. fragilis NrdAB may have a role in maintaining deoxyri
36 he immunomodulatory activities of PSA during B. fragilis colonization include correcting systemic T c
40 ated with diarrheal disease (enterotoxigenic B. fragilis) produce a 20-kDa zinc-dependent metalloprot
42 ssay can be used to identify enterotoxigenic B. fragilis and may be used clinically to determine the
43 hogenicity island (BfPAI) in enterotoxigenic B. fragilis (ETBF) strain 86-5443-2-2 and a related gene
46 diarrhea in children (termed enterotoxigenic B. fragilis, or ETBF) produce a heat-labile ca. 20-kDa p
47 er, the cloning and sequencing of the entire B. fragilis toxin gene (bft) from enterotoxigenic B. fra
48 Deletion of its gene resulted in the first B. fragilis mutant able to synthesize only one phase-var
49 al homologs, allow corrected annotations for B. fragilis bfr and other dpsl genes within the bacteria
56 new, self-transferable transfer factor from B. fragilis LV23 and that this new factor encodes a tetr
59 dynamics of the metallo-beta-lactamase from B. fragilis have been examined using (15)N NMR relaxatio
60 ese data indicate that a purified toxin from B. fragilis strains associated with diarrhea rapidly and
61 biotic colonization of mammals, we generated B. fragilis strains deleted in the global regulator of p
66 supports lipopolysaccharide biosynthesis in B. fragilis and is subject to feedback regulation by CMP
69 te-specific recombinase family, conserved in B. fragilis, mediate additional DNA inversions of the B.
70 psis in mice; however, Fpn is dispensable in B. fragilis colitis, wherein host proteases mediate BFT
71 a single gene, oxe (i.e., oxygen enabled) in B. fragilis allows for growth in concentrations as high
72 brings the total of oxyR-controlled genes in B. fragilis to five and suggests the existence of a seco
77 e global regulatory nature of the process in B. fragilis suggest an evolutionarily ancient mechanism
79 further our understanding of DNA transfer in B. fragilis, we isolated and characterized a new transfe
80 required for GALT development, we introduced B. fragilis along with stress-response mutants of B. sub
81 the distribution and colonization of labeled B. fragilis along the intestine, as well as niche compet
82 sorption studies demonstrate that the native B. fragilis enzyme tightly binds 2 mol of Zn(II) and, al
84 rates of isolation of B. fragilis versus non-B. fragilis species had an overall effect on susceptibil
85 rom DNA extracted from 28 nonenterotoxigenic B. fragilis isolates or B. distasonis, B. thetaiotaomicr
86 cate that whereas both ETBF and nontoxigenic B. fragilis (NTBF) chronically colonize mice, only ETBF
87 udying a collection of ETBF and nontoxigenic B. fragilis (NTBF) strains, we found that bft and a seco
88 ins that do not secrete BFT are nontoxigenic B. fragilis (NTBF), and those that do are called enterot
89 can be transferred from ETBF to nontoxigenic B. fragilis strains by a mechanism similar to that for t
91 symbiosis factor (PSA, polysaccharide A) of B. fragilis signals through TLR2 directly on Foxp3(+) re
93 tive stress are physiological adaptations of B. fragilis to its environment that enhance survival in
94 the role of the CPC in promoting adhesion of B. fragilis to the peritoneal wall and coordinating the
99 nts were designed to determine the effect of B. fragilis enterotoxin on bacteria-enterocyte interacti
105 ich represent 3% of the clinical isolates of B. fragilis, displayed heterogeneity in the regions flan
113 of these findings for the pathophysiology of B. fragilis in extraintestinal infections and competitio
114 In this study, we analysed the phenotype of B. fragilis mutants with defective protein glycosylation
115 lycosylation is central to the physiology of B. fragilis and is necessary for the organism to competi
119 in the number of IRs are active processes of B. fragilis in the endogenous human intestinal ecosystem
121 ulatory molecule, polysaccharide A (PSA), of B. fragilis mediates the conversion of CD4(+) T cells in
123 plots of the deduced amino acid sequence of B. fragilis Omp121 display striking similarity with thos
124 T-ETBF) strains, a nontoxigenic WT strain of B. fragilis (WT-NTBF), WT-NTBF overexpressing bft (rETBF
127 e epidemiology of enterotoxigenic strains of B. fragilis in clinical infections and whether there is
131 esponses specific for B. thetaiotaomicron or B. fragilis were associated with the efficacy of CTLA-4
133 e for commensal bacterial Ags, in particular B. fragilis expressing polysaccharide A, in protecting a
135 e studied the effects of the highly purified B. fragilis fragilysin on the barrier function of cultur
137 2.5 mM, while those of Bacteroides pyogenes, B. fragilis, and Akkermansia muciniphila were greater in
138 To chart the evolution of the more reactive B. fragilis enzyme, we have made changes in an active si
139 f the possibility of metronidazole-resistant B. fragilis strains in the United States and the importa
143 egions of GA3 loci, GA3 T6SSs of the species B. fragilis are likely the source of numerous novel effe
144 polysaccharide complex of a commonly studied B. fragilis strain, 638R, that is distinct from strain 9
145 roximately 6-kb pathogenicity island (termed B. fragilis pathogenicity island or BfPAI) which is pres
147 ca. 20-kDa heat-labile protein toxin (termed B. fragilis toxin [BFT]) have been associated with diarr
151 e deduced amino acid sequences revealed that B. fragilis AhpCF shares approximately 60% identity to o
152 otting and oxyR'::xylB fusions revealed that B. fragilis OxyR does not control its own expression.
154 ansferrin as a model, it has been shown that B. fragilis alone can rapidly and efficiently deglycosyl
160 D Q5LIW1) is the only protein encoded by the B. fragilis genome with significant identity to any know
162 in conferring charged groups that enable the B. fragilis capsular polysaccharides to induce abscesses
163 %) differ greatly from that reported for the B. fragilis chromosome (42%), suggesting that the BfPAI
165 e proposed minimum kinetic mechanism for the B. fragilis metallo-beta-lactamase-catalyzed nitrocefin
166 egions flanking the Tn4400' insertion in the B. fragilis chromosome revealed the presence of five ope
169 ly, by introducing a C104R mutation into the B. fragilis enzyme, binding of two zinc ions is maintain
172 obtained which was confirmed as part of the B. fragilis enterotoxin gene by Southern blotting with a
173 uxs1 is located in a conserved region of the B. fragilis genome, whereas Bfuxs2 is in the heterogeneo
178 was found to be present in the genome of the B. fragilis NCTC9343 strain but absent in strains 638R,
179 report the cloning and overexpression of the B. fragilis phosphonopyruvate decarboxylase gene (aepY),
180 the protein profile of crude extracts of the B. fragilis strains revealed that at least three oxidati
183 ETBF was isolated from 20.3% (40/197) of the B. fragilis-positive diarrheal specimens and from 8.1% (
184 heal specimens and from 8.1% (15/185) of the B. fragilis-positive nondiarrheal specimens (P < .001) a
186 isolation of the various species showed the B. fragilis species comprised 58% of the isolates in 198
187 c-dependent metalloprotease toxin termed the B. fragilis toxin (BFT) have been associated with acute
189 at they are functional paralogs and that the B. fragilis NCTC 9343 PSF repeat unit contains xylose.
190 etic calculations have demonstrated that the B. fragilis protein efficiently binds the internal Na(+)
191 subconfluent HT29/C1 cells treated with the B. fragilis toxin (BFT) develop morphologic changes with
193 -independent IL-10 production in response to B. fragilis during its pathogenic interactions with the
197 20-kDa zinc-dependent metalloprotease toxin (B. fragilis enterotoxin; BFT) that reversibly stimulates
199 ained from mice reconstituted with wild type B. fragilis had significantly enhanced rates of conversi
202 rum reactivity against Bacteroides vulgatus, B. fragilis, Prevotella intermedia, and, to a lesser ext
203 nsferrin deglycosylation occurs in vivo when B. fragilis is propagated in the rat tissue cage model o
204 We identify an alternative pathway by which B. fragilis is able to reestablish capsule production an
205 Monocolonization of germ-free animals with B. fragilis increases the suppressive capacity of Tregs
206 o develop abscesses following challenge with B. fragilis or abscess-inducing zwitterionic polysacchar
208 This defect was overcome by gavage with B. fragilis, by immunization with B. fragilis polysaccha
209 9 enterocytes were incubated for 1 hour with B. fragilis enterotoxin, followed by 1 hour of incubatio
210 avage with B. fragilis, by immunization with B. fragilis polysaccharides, or by adoptive transfer of
211 o was increased in YAMC cells incubated with B. fragilis, an effect mediated by lipopolysaccharide an
212 sphingolipids, we found that treatment with B. fragilis glycosphingolipids-exemplified by an isolate
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