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1                                              B. cenocepacia (genomovar III) is the most prevalent and
2                                              B. cenocepacia can survive intracellularly in macrophage
3                                              B. cenocepacia efficiently activates the inflammasome an
4                                              B. cenocepacia employs a type VI secretion system (T6SS)
5                                              B. cenocepacia strain J2315 was isolated from a CF patie
6                                              B. cenocepacia zmpB and zmpA zmpB mutants had no proteol
7 ution (BMD), and MicroScan WalkAway using 50 B. cenocepacia and 50 B. multivorans isolates collected
8 R-based structural analyses, we identified a B. cenocepacia O-glycosylation (ogc) gene cluster necess
9 ed the efficacy of phage therapy in an acute B. cenocepacia lung infection model.
10                                     Although B. cenocepacia strains can be isolated from soil and can
11 nically relevant species, B. multivorans and B. cenocepacia.
12  to these responses, the interaction between B. cenocepacia and Toll-like receptor 5 (TLR5) was inves
13 ndent production of secondary metabolites by B. cenocepacia strains and suggests future work which co
14 demonstrate that production of ornibactin by B. cenocepacia in response to iron starvation requires t
15 ignal previously not known to be produced by B. cenocepacia as well as pyochelin-type siderophores we
16                    Burkholderia cenocepacia (B. cenocepacia) is an opportunistic bacterium; causing s
17 cies as zmpA and was detected in B. cepacia, B. cenocepacia, B. stabilis, B. ambifaria, and B. pyrroc
18 ere we compare metabolomes of three clinical B. cenocepacia strains in synthetic CF sputum medium (SC
19     Within the Burkholderia cepacia complex, B. cenocepacia is the most common species associated wit
20 ile they share similar genetic compositions, B. cenocepacia and B. multivorans exhibit important diff
21 ectron acceptors under anaerobic conditions, B. cenocepacia and B. multivorans used fermentation rath
22                                BCP-deficient B. cenocepacia exhibit a growth-phase-dependent hypersen
23                      Additionally, different B. cenocepacia secretory systems (T3SS, T4SS, and T6SS)
24            However, the role of GSDMD during B. cenocepacia infection is not yet determined.
25 ition of mROS or the absence of GSDMD during B. cenocepacia infections reduces autophagy which plays
26  receptor 5 (TLR5) contributes to exacerbate B. cenocepacia-induced lung epithelial inflammatory resp
27 t that P. aeruginosa alginate may facilitate B. cenocepacia infection by interfering with host innate
28 e whether P. aeruginosa alginate facilitates B. cenocepacia infection in mice, cystic fibrosis transm
29  their ability to secrete IL-1beta following B. cenocepacia infection, suggesting that a deficiency i
30 e plasmid-borne ORFs, carried by pBCA072 for B. cenocepacia J2315 and pESBL for E. coli O104:H4.
31 vity of TecA is necessary and sufficient for B. cenocepacia-triggered lung inflammation and also prot
32 pid A explaining the ability of hypoacylated B. cenocepacia LPS to promote proinflammatory responses
33  or transport appears to dramatically impact B. cenocepacia viability, supporting the assignment of o
34 pid A, suggesting lipid A penta-acylation in B. cenocepacia is required not only for bacterial growth
35 nto the control of cable pilus biogenesis in B. cenocepacia and provide evidence for regulation of cb
36 lagellin subunit, fliCII, was constructed in B. cenocepacia K56-2 and tested in a murine agar bead mo
37 dy highlights strain specific differences in B. cenocepacia virulence mechanisms important for unders
38 ression of cable pilus biosynthetic genes in B. cenocepacia.
39 n model, indicating that zmpB is involved in B. cenocepacia virulence.
40 he role of the PI3K/Akt signaling pathway in B. cenocepacia-infected monocytes and macrophages.
41 s a natural substrate for the efflux pump in B. cenocepacia and imply that the environment of low iro
42 our highly conserved periplasmic residues in B. cenocepacia ArnT, tyrosine-43, lysine-69, arginine-25
43 identified functional pathways that indicate B. cenocepacia can produce a wider array of virulence fa
44 an pyrin is required to detect intracellular B. cenocepacia leading to IL-1beta processing and releas
45              We also show that intracellular B. cenocepacia within macrophages produced more penta-ac
46                             To acquire iron, B. cenocepacia secretes the Fe(III)-binding compound, or
47 growth capabilities of B. cenocepacia J2315, B. cenocepacia K56-2, and B. multivorans ATCC 17616 on 1
48 lammation and also protects mice from lethal B. cenocepacia infection.
49 developing selective inhibitors for limiting B. cenocepacia infection.
50 ole of Cbl pili and the adhesin in mediating B. cenocepacia binding to and transmigration across squa
51                    In contrast to the native B. cenocepacia enzyme, thioredoxin is the preferred redo
52  lectins LecB (P. aeruginosa) and BC2L-C-Nt (B. cenocepacia).
53 tate (3-OH C14:0) relative to the lipid A of B. cenocepacia LMG 12614.
54 rst comprehensive genome-phenome analyses of B. cenocepacia infection in cystic fibrosis lungs and se
55 edictions to in vitro growth capabilities of B. cenocepacia J2315, B. cenocepacia K56-2, and B. multi
56 g and transmigration or invasion capacity of B. cenocepacia.
57            To understand the contribution of B. cenocepacia flagella to infection, a strain mutated i
58 ched in intergenic regions in the genomes of B. cenocepacia strains.
59                                 Ingestion of B. cenocepacia independently contributes to and worsens
60  seven lacZ fusions in a clinical isolate of B. cenocepacia that are inducible by octanoyl-HSL.
61 s were infected with CF clinical isolates of B. cenocepacia and P. aeruginosa.
62 ne and M3 significantly increased killing of B. cenocepacia and P. aeruginosa in CF MDMs in a dose-de
63          (R)-roscovitine-mediated killing of B. cenocepacia was enhanced by combination with the CFTR
64  By immunoscreening an expression library of B. cenocepacia isolate BC7, we identified a large gene (
65 man, J2315 is representative of a lineage of B. cenocepacia rarely isolated from the environment and
66 ells infected with T6SS-defective mutants of B. cenocepacia, suggesting that the inflammatory reactio
67  Further, alginate decreased phagocytosis of B. cenocepacia by professional phagocytes both in vivo a
68 k confirmed the proinflammatory potential of B. cenocepacia penta-acylated lipid A.
69 ts show that the intracellular processing of B. cenocepacia is similar in both professional and nonpr
70 lar survival, replication, and processing of B. cenocepacia.
71 ing to CK13 and transmigration properties of B. cenocepacia.
72 e-scale metabolic network reconstructions of B. cenocepacia J2315 and B. multivorans ATCC 17616 in pa
73 ntributes to the survival and replication of B. cenocepacia in eukaryotic cells.
74 nce of GSDMD-mediated mROS in restriction of B. cenocepacia.
75 ss differential expression, protein spots of B. cenocepacia and B. multivorans that were unique or di
76                           Certain strains of B. cenocepacia express peritrichous adherence organelles
77  is unique in comparison to other strains of B. cenocepacia, highlighting the genomic plasticity of t
78            We examined the transmigration of B. cenocepacia through polarized respiratory epithelium.
79 fied as being required for full virulence of B. cenocepacia K56-2.
80 C biosynthesis genes (ogcI and ogcB) reduces B. cenocepacia viability.
81 million bases of cDNA from 2 closely related B. cenocepacia strains (one isolated from a CF patient a
82 tro findings and showed that GSDMD restricts B. cenocepacia infection and dissemination and stimulate
83 ur in vitro study shows that GSDMD restricts B. cenocepacia replication within macrophages independen
84 remain confined to the endobronchial spaces, B. cenocepacia can traverse airway epithelium to cause b
85            We purified LPS from two strains, B. cenocepacia LMG 12614 and B. multivorans LMG 14273, e
86 ce were differentially regulated, suggesting B. cenocepacia experiences a dramatic shift in metabolis
87     Together, these results demonstrate that B. cenocepacia flagella contribute to virulence in an in
88            In this study, we determined that B. cenocepacia has an additional metalloprotease, which
89                 Recent studies indicate that B. cenocepacia survives within macrophages and airway ep
90 which supports the clinical observation that B. cenocepacia is more virulent than B. multivorans.
91                In this study, we report that B. cenocepacia flagellin is glycosylated on at least 10
92                         Here, we report that B. cenocepacia has only one late acyltransferase, LpxL (
93                         Here, we report that B. cenocepacia LPS strongly activates human TLR4.MD-2 de
94              These observations suggest that B. cenocepacia traverses polarized respiratory epitheliu
95                                          The B. cenocepacia cblBACDS operon encodes the structural an
96 hains and the aminoarabinose residues in the B. cenocepacia lipid A allow exposure of the fifth acyl
97 gulated and upregulated respectively, in the B. cenocepacia proteome.
98                      We demonstrate that the B. cenocepacia BCP (BcBCP) homologue functions through a
99             Our results demonstrate that the B. cenocepacia cblS, cblT, and cblR genes are essential
100 nome of the previously described therapeutic B. cenocepacia podophage BcepIL02 and its close relative
101 esponses of human airway epithelial cells to B. cenocepacia infection.
102 epithelial cells and alveolar macrophages to B. cenocepacia infection.
103 tivation and IL-1beta release in response to B. cenocepacia challenge.
104 uble-edged functions of GSDMD in response to B. cenocepacia infection and shows the importance of GSD
105   GSDMD promotes inflammation in response to B. cenocepacia through mediating the release of inflamma
106 ung inflammation and necrosis in response to B. cenocepacia without altering mice survival.
107 or ASC induced a robust IL-1beta response to B. cenocepacia, which correlated with enhanced host cell
108 tion and stimulates autophagy in response to B. cenocepacia.
109 to airway infections, yet their responses to B. cenocepacia have not been fully investigated.
110 pression of either cblS or cblR in wild-type B. cenocepacia strain BC7 led to a significant increase,
111  for controlling excessive inflammation upon B. cenocepacia infection.
112           While genetic variation in various B. cenocepacia strains has been reported, it remains unc
113 activity within and between genomovars, with B. cenocepacia strains possessing the greatest cytokine
114 P-pyrin and ASC (YFP-ASC) were infected with B. cenocepacia and analyzed for inflammasome activation.
115 e regulator knockout mice were infected with B. cenocepacia strain BC7 suspended in either phosphate-
116 riments revealed that patients infected with B. cenocepacia, Burkholderia multivorans, B. pseudomalle
117 hat in human mononuclear cells infected with B. cenocepacia, pyrin associates with caspase-1 and ASC
118 inflammatory cytokines during infection with B. cenocepacia.
119 pathway during infection of macrophages with B. cenocepacia.

 
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