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1                                              B. mallei and B. pseudomallei are closely related geneti
2                                              B. mallei possesses two glmS genes on chromosome 1 and T
3                                              B. mallei, the etiologic agent of glanders, has come und
4                    The database includes 143 B. mallei proteins associated with five secretion system
5 atabase contains updated information for 163 B. mallei proteins from the previous database and 61 add
6 b 16S rRNA gene of 56 B. pseudomallei and 23 B. mallei isolates selected to represent a wide range of
7 ems with 58 Burkholderia pseudomallei and 23 B. mallei strains for identification of these agents, bu
8                             Twenty-two of 23 B. mallei isolates showed 16S rRNA gene sequence identit
9  42 virulence attenuation experiments for 27 B. mallei secretion system proteins.
10  82 virulence attenuation experiments for 52 B. mallei secretion system proteins and 98 virulence att
11 HSL profiles from B. mallei ATCC 23344 and a B. mallei bmaI1 mutant indicates that octanoyl-HSL synth
12  by comparison with bacteriophage phiE125, a B. mallei-specific bacteriophage produced by Burkholderi
13 ount a durable adaptive immune response to a B. mallei infection.
14 nd computationally derived information about B. mallei ATCC 23344 and literature-based and computatio
15 nd computationally derived information about B. mallei strain ATCC 23344.
16 e conclude that QS is not required for acute B. mallei infections of mice.
17 from the previous database and 61 additional B. mallei proteins, and new information for 281 B. pseud
18 on of IL-12 and IFN-gamma in the lungs after B. mallei infection was significantly impaired in both M
19 ng mechanisms of protective immunity against B. mallei and B. pseudomallei, including antigen discove
20 y be important for immune protection against B. mallei infection.
21  genetic manipulation of B. pseudomallei and B. mallei and currently few reliable tools for the genet
22                Burkholderia pseudomallei and B. mallei are bacterial pathogens that cause melioidosis
23 ed virulence features of B. pseudomallei and B. mallei are discussed.
24                Burkholderia pseudomallei and B. mallei are Gram-negative bacterial pathogens that cau
25             In contrast, B. pseudomallei and B. mallei BimA mimic host Ena/VASP actin polymerases in
26 -related genes shared by B. pseudomallei and B. mallei but not present in five closely related nonpat
27 ying and differentiating B. pseudomallei and B. mallei by molecular methods.
28 haridic fragments of the B. pseudomallei and B. mallei CPS repeating unit is reported.
29 ion of the select agents B. pseudomallei and B. mallei using allelic exchange.
30 hese genes contribute to B. pseudomallei and B. mallei virulence.
31 gate host; we found that B. pseudomallei and B. mallei, but not other phylogenetically related bacter
32                Burkholderia pseudomallei and B. mallei, the causative agents of melioidosis and gland
33 tool for differentiating B. pseudomallei and B. mallei, two closely related biological threat agents.
34 e to the pathogenesis of B. pseudomallei and B. mallei.
35  genes in the genomes of B. pseudomallei and B. mallei.
36  genetic manipulation of B. pseudomallei and B. mallei.
37 landensis is a nonpathogenic saprophyte, and B. mallei is a host-restricted pathogen.
38           Utilizing the B. thailandensis and B. mallei lipopolysaccharide (LPS)-specific monoclonal a
39 ns of B. pseudomallei, B. thailandensis, and B. mallei serves as a platform for predicting which QS-c
40 s for B. pseudomallei, B. thailandensis, and B. mallei, these patterns differed from those of other B
41 ia caused by gram-negative bacteria, such as B. mallei, has not been assessed.
42 es for which genome sequences are available, B. mallei, B. pseudomallei, and B. cepacia, are predicte
43  been reported previously: BimA(Bp) and BimA B. mallei-like (BimA(Bm)).
44 fic protection from aerosol exposure to both B. mallei and B. pseudomallei.
45 e antigenically similar to those produced by B. mallei ATCC 23344.
46 her host proteins that were also targeted by B. mallei proteins.
47 e importantly, four previously characterized B. mallei mutants with reduced virulence in hamsters or
48 on observed with the P. aeruginosa, E. coli, B. mallei, and G. intestinalis ADIs.
49 ice were vaccinated twice with the different B. mallei preparations, and spleens and sera were collec
50                              Three different B. mallei cell preparations plus Alhydrogel were evaluat
51  role of gamma interferon (IFN-gamma) during B. mallei infection was investigated using a disease mod
52 dy, we constructed the select-agent-excluded B. mallei DeltatonB Deltahcp1 (CLH001) vaccine strain an
53 -) mice, compared with WT animals, following B. mallei challenge.
54 s producing IFN-gamma in the lungs following B. mallei infection, while DCs and monocytes were the pr
55 in comparison with that in WT mice following B. mallei infection, whereas neutrophil recruitment was
56 about 13 pathogenic mechanisms of action for B. mallei and B. pseudomallei secretion system proteins
57 about 10 pathogenic mechanisms of action for B. mallei secretion system proteins inferred from the av
58                        Selection markers for B. mallei are limited to Km and Zeo resistance genes.
59  progress, the secretion system proteins for B. mallei and B. pseudomallei, their pathogenic mechanis
60  identities of secretion system proteins for B. mallei are not well known, and their pathogenic mecha
61 , of bacterial secretion system proteins for B. mallei.
62  delineate the relevant acyl-HSL signals for B. mallei LuxR homologs, we analyzed the BmaR1-BmaI1 sys
63       A comparison of acyl-HSL profiles from B. mallei ATCC 23344 and a B. mallei bmaI1 mutant indica
64 responses required for early protection from B. mallei infection.
65 seudomallei are closely related genetically; B. mallei evolved from an ancestral strain of B. pseudom
66 d murine-interacting targets, and 2,400 host-B. mallei interactions and 2,286 host-B. pseudomallei in
67 ng targets, and the corresponding 2,400 host-B. mallei interactions.
68 utants in B. pseudomallei, and one mutant in B. mallei.
69   Furthermore, we assessed the role of QS in B. mallei ATCC 23344 by constructing and characterizing
70 in in-depth information on the role of QS in B. mallei virulence, we constructed and characterized a
71 ol for application of the mini-Tn7 system in B. mallei as an example of bacteria with multiple glmS s
72  This first chromosome integration system in B. mallei provides an important contribution to the gene
73 Tn7 site-specific transposition pathway into B. mallei by conjugation, followed by selection of inser
74 ma production in the presence of heat-killed B. mallei.
75 -gamma production in response to heat-killed B. mallei.
76 , and effective at protecting against lethal B. mallei challenge.
77 ormed an extended analysis of primarily nine B. mallei virulence factors and their interactions with
78 xed T-helper-cell-like response to nonviable B. mallei is obtained, as demonstrated by a Th1- and Th2
79 lational challenge with 100% lethal doses of B. mallei and B. pseudomallei.
80 stem is required for intracellular growth of B. mallei in J774.2 cells, formation of macrophage membr
81 ere initiated to examine the interactions of B. mallei tssE mutants with RAW 264.7 murine macrophages
82 rities between host-pathogen interactions of B. mallei, Yersinia pestis, and Salmonella enterica.
83 we constructed and characterized a mutant of B. mallei strain GB8 that was unable to make acyl-homose
84 (s) that contributes to the pathogenicity of B. mallei in vivo.
85                We inferred putative roles of B. mallei proteins based on the roles of their aligned Y
86  provide a safe and cost-effective source of B. mallei-like OPS to facilitate the synthesis of glande
87 useful in identifying unsequenced strains of B. mallei and B. pseudomallei.
88 specifically in PhiE125 lysogenic strains of B. mallei and Burkholderia thailandensis, revealed that,
89 nsive information about secretion systems of B. mallei and B. pseudomallei.
90 s a role in the intracellular trafficking of B. mallei and may facilitate cell-to-cell spread via act
91 and actin-based motility following uptake of B. mallei by RAW 264.7 cells.
92 ene was expressed within 1 h after uptake of B. mallei into RAW 264.7 murine macrophages, suggesting
93 ermine if QS is involved in the virulence of B. mallei, we generated mutations in each putative luxIR
94 quired to generate protection from pneumonic B. mallei infection.
95 okine required for protection from pneumonic B. mallei infection.
96                In a mouse model of pneumonic B. mallei infection, we found that both MCP-1(-/-) mice
97 unknown, the TssM deubiquitinase may provide B. mallei a selective advantage in the intracellular env
98 bability virulence genes in B. pseudomallei, B. mallei, and other pathogens.
99 pp. that includes Burkholderia pseudomallei, B. mallei, and B. thailandensis.
100  Burkholderia pseudomallei and its relatives B. mallei, B. oklahomensis, and B. thailandensis.
101 nes required for protection from respiratory B. mallei infection.
102 n, although devoid of hexa-acylated species, B. mallei LPS was shown to be a potent activator of huma
103 al analyses and MALDI-TOF mass spectrometry, B. mallei was shown to express a heterogeneous mixture o
104    Based upon these results, it appears that B. mallei LPS is likely to play a significant role in th
105              These findings demonstrate that B. mallei carries multiple luxIR homologues that either
106                           Our data show that B. mallei is susceptible to cell-mediated immune respons
107                                 We show that B. mallei produces N-3-hydroxy-octanoyl HSL (3OHC8-HSL)
108                                          The B. mallei tssM gene encodes a putative ubiquitin-specifi
109                                          The B. mallei VirAG two-component regulatory system activate
110                                 Although the B. mallei VirAG two-component regulatory system is requi
111 a mallei produces several acyl-HSLs, and the B. mallei genome has four luxR and two luxI homologs, ea
112                                      For the B. mallei transcriptional regulator mutants (luxR homolo
113 tations (disruption of bsaQ and bsaZ) in the B. mallei ATCC 23344 animal pathogen-like type III secre
114 s may be the reason for the inability of the B. mallei cells that were examined as candidate vaccines
115                            Disruption of the B. mallei QS alleles, especially in RJ16 (bmaII) and RJ1
116 by the oacA mutant reacted strongly with the B. mallei LPS-specific protective monoclonal antibody 9C
117  protected against lethal challenge with the B. mallei lux (CSM001) wild-type strain.
118 RJ20 (bmaR5) (151 CFU) compared to wild-type B. mallei (<13 CFU).
119 ction, we determined the LD50s for wild-type B. mallei and each QS mutant.
120  mass spectrometry, we showed that wild-type B. mallei produces the signaling molecules N-octanoyl-ho
121 , immunoblot analyses demonstrated that when B. mallei ATCC 23344 was complemented in trans with oacA
122 ental and computational data associated with B. mallei secretion systems.
123 ghly susceptible to pulmonary challenge with B. mallei and had significantly short survival times, in
124 ection against lethal aerosol challenge with B. mallei ATCC 23344, it also protects against infection
125 red protection against lethal challenge with B. mallei.
126        IFN-gamma knockout mice infected with B. mallei died within 2 to 3 days after infection, and t
127 roduction following pneumonic infection with B. mallei and therefore may also figure importantly in o
128 mely susceptible to pulmonary infection with B. mallei, compared with wild-type (WT) C57Bl/6 mice.
129 tective immunity to pulmonary infection with B. mallei.

 
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