ライフサイエンスコーパス: B. melitensis

1 ificantly elevated upon removal of bioR from B. melitensis.

2 y of novel vaccines and therapeutics against B. melitensis.

3 against inhalational infection with virulent B. melitensis.

4 ting against intracellular organisms such as B. melitensis.

5 e against intranasal challenge with virulent B. melitensis.

6 Using the B. melitensis 16 M genome sequence, primers were designe

7 d in identifying genomic differences between B. melitensis 16M and Brucella abortus 2308.

8 re were both pro- and antiapoptosis effects, B. melitensis 16M appears to inhibit apoptosis of macrop

9 that (i) OPS-deficient strains derived from B. melitensis 16M are more resistant to the bactericidal

10 otect mice against intranasal challenge with B. melitensis 16M bacteria.

11 y this, deletion mutants were constructed in B. melitensis 16M by removing genes encoding phosphomann

12 mutant improved protection against wild-type B. melitensis 16M challenge compared to the nonencapsula

13 Deletion of wboA in smooth, virulent B. melitensis 16M results in a rough mutant designated W

14 After challenge with B. melitensis 16M strain, two protective antigens were f

15 ies, we used the complete genome sequence of B. melitensis 16M, the species highly pathogenic to huma

16 ted mice upon nasal challenge with wild-type B. melitensis 16M.

17 6 animals after intranasal administration of B. melitensis 16M.

18 otect mice against intranasal challenge with B. melitensis 16M.

19 hybridization led to our conclusion that the B. melitensis 28-kDa protein was a group 3 protein disti

20 To investigate the role of cyclic-di-GMP in B. melitensis, all 11 predicted cyclic-di-GMP-metabolizi

21 severity as WT mice following infection with B. melitensis and treatment with anti-IFN-gamma.

22 Brucella abortus, B. melitensis, and B. suis are pathogenic to humans, whe

23 spensable for the persistence of B. abortus, B. melitensis, and B. suis in mice up to 4 weeks after i

24 is a rodent pathogen, and unlike B. abortus, B. melitensis, and B. suis, B. neotomae has not been obs

25 ree pathogenic Brucella species: B. abortus, B. melitensis, and B. suis.

26 on susceptibility tests of Brucella abortus, B. melitensis, and B. suis.

27 omplement fixation tests with B. abortus and B. melitensis antigens (CFA and CFM), USDA and Mexican m

28 Three patterns of antibody responses against B. melitensis antigens were seen for serum samples obtai

29 quired for food-borne infection of humans by B. melitensis are poorly understood.

30 B. abortus, both smooth and rough strains of B. melitensis are resistant to complement-mediated killi

31 c infections with either Brucella abortus or B. melitensis at various doses.

32 he homologous sequences of Brucella abortus, B. melitensis, B. canis, and B. suis.

33 d animal origin, including Brucella abortus, B. melitensis, B. ovis, B. neotomae, marine mammal isola

34 B. abortus, B. melitensis, B. suis, and B. canis produced identical

35 s of five Brucella species-Brucella abortus, B. melitensis, B. suis, B. canis, and B. ovis-using whol

36 me for the detection of Brucella melitensis (B. melitensis) based on the screening of its complementa

37 sts that the presence of surface OPS on live B. melitensis benefits the bacterium by preventing the d

38 The B. melitensis BioR ortholog was overexpressed and purifi

39 Furthermore, B. melitensis but not B. abortus nor B. suis interfered

40 ine whether oral administration of DeltaznuA B. melitensis can confer protection against nasal B. mel

41 litensis can confer protection against nasal B. melitensis challenge.

42 attenuation displayed by this strain and its B. melitensis counterpart in experimentally infected ani

43 RMs given an aerosol challenge with B. melitensis developed undulating fevers (6/6 phase I;

44 We have investigated how B. suis and B. melitensis enter human monocytes and in which compart

45 ve limited ability to control infection with B. melitensis, even when activated by IFN-gamma in the p

46 d host range (e.g., Brucella suis for swine, B. melitensis for sheep and goats, and Brucella abortus

47 Several features of the B. melitensis genome are similar to those of the symbiot

48 tification of Brucella spp., B. abortus, and B. melitensis in a single test.

49 ides an alternative way for the detection of B. melitensis in less than 10min.

50 Joints from B. melitensis-infected IFN-gamma(-/-) mice had markedly

51 In contrast, B. melitensis infection diminishes more rapidly, and hig

52 pproaches to classifying and prognosticating B. melitensis infection have ever been delineated.

53 Few cases of B. melitensis infection in goats have occurred in the Un

54 confer protective immunity in the spleen to B. melitensis infection.

55 lay an important role in the pathogenesis of B. melitensis infection.

56 These results indicate that B. melitensis is able to spread systemically from the di

57 In contrast to B. suis and B. melitensis, it was found that B. neotomae is a partia

58 quences were identical and differed from the B. melitensis IVS sequences by a single base pair.

59 n this study, chronic infection of mice with B. melitensis led to CD8(+) T cell exhaustion, manifeste

60 ulin G (IgG) and IgA antibodies specific for B. melitensis LPS in lung lavages and specific IgG and I

61 udies show that intranasal immunization with B. melitensis LPS-GBOMP subunit vaccine significantly pr

62 us, which shares an immunogenic epitope with B. melitensis LPS.

63 nts are the first to systematically identify B. melitensis MHC-II-restricted CD4(+) T cell epitopes r

64 ogenicity of three attenuated bioluminescent B. melitensis mutants, GR019 (virB4), GR024 (galE), and

65 e bactericidal action of NHS than were rough B. melitensis mutants.

66 nst killed B. abortus whole cells recognized B. melitensis Omp28 on Western blots (immunoblots).

67 ups of 10 goats experimentally infected with B. melitensis or B. abortus and monitored for 24 weeks.

68 mary and secondary intranasal infection with B. melitensis Our analysis of primary infection demonstr

69 ce and goats infected with smooth strains of B. melitensis produced Abs against Omp28.

70 A B. melitensis protein microarray comprised of nearly all

71 nized by IgG in human sera on a genome level B. melitensis protein microarray.

72 We designated the B. melitensis protein Omp28.

73 Four peptide epitopes derived from 3 B. melitensis proteins (BMEI 1330, a DegP/HtrA protease;

74 as confirmed with DNA vaccines for these two B. melitensis proteins and, when combined, protection ag

75 onic brucellosis recognized some of the same B. melitensis proteins as those recognized by sera from

76 Computer-assisted analysis of the two B. melitensis proteomes revealed proteins expressed in e

77 A single oral vaccination with DeltaznuA B. melitensis rapidly cleared from mice within 2 weeks a

78 onfirming these results, deletion of blxR in B. melitensis reduced the transcriptional activities of

79 iated protein 1-positive inclusions, whereas B. melitensis replicated in the ER-derived compartment.

80 neotomae by using nirK, nirV, and nnrA from B. melitensis restored the ability of B. neotomae to red

81 A low dose of 1000 cfu/animal of B. melitensis resulted in 45% of mice with tissue burden

82 Genome sequencing of B. suis and B. melitensis revealed that both are complete denitrifie

83 ice inoculated with B. abortus 19 or 2308 or B. melitensis RM1 also produced antibodies to YajC.

84 rts previous indications that B. abortus and B. melitensis share a common ancestor that diverged from

85 osorbent assay (iELISA) for the detection of B. melitensis-specific antibodies in goat milk.

86 use as a bulk milk test for the detection of B. melitensis-specific antibodies in goat milk.

87 The B. melitensis-specific CD8(+) T cells that produced IFN-

88 nged intranasally with 10(4) CFU of virulent B. melitensis strain 16 M 4 weeks after the second dose

89 . suis strain 1330 but no protection against B. melitensis strain 16 M.

90 e were challenged intranasally with virulent B. melitensis strain 16M 4 weeks after the second dose o

91 B. melitensis strain 16M was consistently recovered from

92 The genome of B. melitensis strain 16M was sequenced and found to cont

93 s in the epidemiological genotyping of human B. melitensis strains.

94 The mechanism by which B. melitensis subverts adaptive immunological memory is

95 Smooth B. melitensis survived and multiplied for at least 6 day

96 and had fewer nucleotide polymorphisms with B. melitensis than B. suis.

97 l deletions on chromosomes of B. abortus and B. melitensis that encoded proteins of various metabolic

98 To understand the mechanism of virulence in B. melitensis, the proteome of vaccine strain Rev 1 was

99 vitro lymphoepithelial cell (M-cell) model, B. melitensis transited rapidly through polarized entero

100 nization with the live, attenuated DeltaznuA B. melitensis vaccine provides an attractive strategy to

101 ly identified as unique to either B. suis or B. melitensis were present in the B. abortus genome.

102 blxR mutant was similar to that of wild-type B. melitensis, while the vjbR mutant was defective for s

103 e role of surface OPS in the interactions of B. melitensis with monocytes/macrophages (M/M), 16M and

104 istered live, attenuated, purine auxotrophic B. melitensis WR201 bacteria for their ability to elicit