ライフサイエンスコーパス: B. mallei

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 ia caused by gram-negative bacteria, such as B. mallei, has not been assessed.

41 es for which genome sequences are available, B. mallei, B. pseudomallei, and B. cepacia, are predicte

42 fic protection from aerosol exposure to both B. mallei and B. pseudomallei.

43 e antigenically similar to those produced by B. mallei ATCC 23344.

44 her host proteins that were also targeted by B. mallei proteins.

45 e importantly, four previously characterized B. mallei mutants with reduced virulence in hamsters or

46 on observed with the P. aeruginosa, E. coli, B. mallei, and G. intestinalis ADIs.

47 ice were vaccinated twice with the different B. mallei preparations, and spleens and sera were collec

48 Three different B. mallei cell preparations plus Alhydrogel were evaluat

49 role of gamma interferon (IFN-gamma) during B. mallei infection was investigated using a disease mod

50 dy, we constructed the select-agent-excluded B. mallei DeltatonB Deltahcp1 (CLH001) vaccine strain an

51 -) mice, compared with WT animals, following B. mallei challenge.

52 s producing IFN-gamma in the lungs following B. mallei infection, while DCs and monocytes were the pr

53 in comparison with that in WT mice following B. mallei infection, whereas neutrophil recruitment was

54 about 13 pathogenic mechanisms of action for B. mallei and B. pseudomallei secretion system proteins

55 about 10 pathogenic mechanisms of action for B. mallei secretion system proteins inferred from the av

56 Selection markers for B. mallei are limited to Km and Zeo resistance genes.

57 progress, the secretion system proteins for B. mallei and B. pseudomallei, their pathogenic mechanis

58 identities of secretion system proteins for B. mallei are not well known, and their pathogenic mecha

59 , of bacterial secretion system proteins for B. mallei.

60 delineate the relevant acyl-HSL signals for B. mallei LuxR homologs, we analyzed the BmaR1-BmaI1 sys

61 A comparison of acyl-HSL profiles from B. mallei ATCC 23344 and a B. mallei bmaI1 mutant indica

62 responses required for early protection from B. mallei infection.

63 seudomallei are closely related genetically; B. mallei evolved from an ancestral strain of B. pseudom

64 d murine-interacting targets, and 2,400 host-B. mallei interactions and 2,286 host-B. pseudomallei in

65 ng targets, and the corresponding 2,400 host-B. mallei interactions.

66 utants in B. pseudomallei, and one mutant in B. mallei.

67 Furthermore, we assessed the role of QS in B. mallei ATCC 23344 by constructing and characterizing

68 in in-depth information on the role of QS in B. mallei virulence, we constructed and characterized a

69 ol for application of the mini-Tn7 system in B. mallei as an example of bacteria with multiple glmS s

70 This first chromosome integration system in B. mallei provides an important contribution to the gene

71 Tn7 site-specific transposition pathway into B. mallei by conjugation, followed by selection of inser

72 ma production in the presence of heat-killed B. mallei.

73 -gamma production in response to heat-killed B. mallei.

74 , and effective at protecting against lethal B. mallei challenge.

75 ormed an extended analysis of primarily nine B. mallei virulence factors and their interactions with

76 xed T-helper-cell-like response to nonviable B. mallei is obtained, as demonstrated by a Th1- and Th2

77 lational challenge with 100% lethal doses of B. mallei and B. pseudomallei.

78 stem is required for intracellular growth of B. mallei in J774.2 cells, formation of macrophage membr

79 ere initiated to examine the interactions of B. mallei tssE mutants with RAW 264.7 murine macrophages

80 rities between host-pathogen interactions of B. mallei, Yersinia pestis, and Salmonella enterica.

81 we constructed and characterized a mutant of B. mallei strain GB8 that was unable to make acyl-homose

82 (s) that contributes to the pathogenicity of B. mallei in vivo.

83 We inferred putative roles of B. mallei proteins based on the roles of their aligned Y

84 provide a safe and cost-effective source of B. mallei-like OPS to facilitate the synthesis of glande

85 useful in identifying unsequenced strains of B. mallei and B. pseudomallei.

86 specifically in PhiE125 lysogenic strains of B. mallei and Burkholderia thailandensis, revealed that,

87 nsive information about secretion systems of B. mallei and B. pseudomallei.

88 s a role in the intracellular trafficking of B. mallei and may facilitate cell-to-cell spread via act

89 and actin-based motility following uptake of B. mallei by RAW 264.7 cells.

90 ene was expressed within 1 h after uptake of B. mallei into RAW 264.7 murine macrophages, suggesting

91 ermine if QS is involved in the virulence of B. mallei, we generated mutations in each putative luxIR

92 quired to generate protection from pneumonic B. mallei infection.

93 okine required for protection from pneumonic B. mallei infection.

94 In a mouse model of pneumonic B. mallei infection, we found that both MCP-1(-/-) mice

95 unknown, the TssM deubiquitinase may provide B. mallei a selective advantage in the intracellular env

96 bability virulence genes in B. pseudomallei, B. mallei, and other pathogens.

97 pp. that includes Burkholderia pseudomallei, B. mallei, and B. thailandensis.

98 Burkholderia pseudomallei and its relatives B. mallei, B. oklahomensis, and B. thailandensis.

99 nes required for protection from respiratory B. mallei infection.

100 n, although devoid of hexa-acylated species, B. mallei LPS was shown to be a potent activator of huma

101 al analyses and MALDI-TOF mass spectrometry, B. mallei was shown to express a heterogeneous mixture o

102 Based upon these results, it appears that B. mallei LPS is likely to play a significant role in th

103 These findings demonstrate that B. mallei carries multiple luxIR homologues that either

104 Our data show that B. mallei is susceptible to cell-mediated immune respons

105 We show that B. mallei produces N-3-hydroxy-octanoyl HSL (3OHC8-HSL)

106 The B. mallei tssM gene encodes a putative ubiquitin-specifi

107 The B. mallei VirAG two-component regulatory system activate

108 Although the B. mallei VirAG two-component regulatory system is requi

109 a mallei produces several acyl-HSLs, and the B. mallei genome has four luxR and two luxI homologs, ea

110 For the B. mallei transcriptional regulator mutants (luxR homolo

111 tations (disruption of bsaQ and bsaZ) in the B. mallei ATCC 23344 animal pathogen-like type III secre

112 s may be the reason for the inability of the B. mallei cells that were examined as candidate vaccines

113 Disruption of the B. mallei QS alleles, especially in RJ16 (bmaII) and RJ1

114 by the oacA mutant reacted strongly with the B. mallei LPS-specific protective monoclonal antibody 9C

115 protected against lethal challenge with the B. mallei lux (CSM001) wild-type strain.

116 RJ20 (bmaR5) (151 CFU) compared to wild-type B. mallei (<13 CFU).

117 ction, we determined the LD50s for wild-type B. mallei and each QS mutant.

118 mass spectrometry, we showed that wild-type B. mallei produces the signaling molecules N-octanoyl-ho

119 , immunoblot analyses demonstrated that when B. mallei ATCC 23344 was complemented in trans with oacA

120 ental and computational data associated with B. mallei secretion systems.

121 ghly susceptible to pulmonary challenge with B. mallei and had significantly short survival times, in

122 ection against lethal aerosol challenge with B. mallei ATCC 23344, it also protects against infection

123 red protection against lethal challenge with B. mallei.

124 IFN-gamma knockout mice infected with B. mallei died within 2 to 3 days after infection, and t

125 roduction following pneumonic infection with B. mallei and therefore may also figure importantly in o

126 mely susceptible to pulmonary infection with B. mallei, compared with wild-type (WT) C57Bl/6 mice.

127 tective immunity to pulmonary infection with B. mallei.