ライフサイエンスコーパス: R. equi

1 R. equi CFS was also examined for the ability to stimula

2 R. equi virulence is dependent on the presence of a larg

3 R. equi-stimulated peripheral blood mononuclear cells (P

4 A TRAVAP survey of 215 R. equi strains confirmed the strong link between vapA (

5 In contrast, mice transfused with a R. equi-specific CD4+ Th2 cell line expressed interleuki

6 xamine the mechanism of host defense against R. equi by using a murine model.

7 ets in the immunoprotective response against R. equi infection.

8 Although R. equi infection can produce life-threatening pyogranul

9 We subsequently constructed an R. equi strain lacking only the vapA gene and found that

10 is study, we describe the construction of an R. equi mutant lacking a 7.9 kb DNA region spanning five

11 In these assays, R. equi remains fully viable following prolonged exposur

12 A TLR2 reporter cell was activated by R. equi, and RAW-264 cells transfected with a dominant n

13 e efficient activation of innate immunity by R. equi may account for the relative lack of virulence o

14 m of TLR4 responded normally to infection by R. equi.

15 This "TRAVAP" typing scheme classifies R. equi into 4 categories: traA(+)/vapA(+)B(-), traA(+)/

16 cient to confer virulence to a plasmid-cured R. equi recipient.

17 mid-containing) or avirulent (plasmid-cured) R. equi.

18 face and at the membrane of the host-derived R. equi containing vacuole, thus providing an opportunit

19 te that immunocompetent adult horses develop R. equi-specific CD8+ CTL, which may play a role in immu

20 ype mice blocked lesion regression following R. equi infection.

21 polymerase chain reaction typing system for R. equi based on 3 plasmid gene markers: traA from the c

22 g strains of R. equi (donor) to plasmid-free R. equi strains (recipient) at a high frequency and that

23 and 24 kDa and were recognized by sera from R. equi-infected foals and immune adult horses.

24 coccus equi and specifically to determine if R. equi-specific CD8+ CTL occurred in the blood of immun

25 vapC, -D, and -E are found only in R. equi strains that express VapA and are highly conserv

26 tudy showing a virulence plasmid transfer in R. equi, and it establishes a mechanism by which the vir

27 We show that Himar1 transposition in R. equi is random and needs no apparent consensus sequen

28 to form peroxynitrite (ONOO(-)), which kills R. equi.

29 p91(phox-/-)) are more susceptible to lethal R. equi infection and display higher bacterial burdens i

30 The role of the surface-localized R. equi lipoprotein VapA (virulence-associated protein A

31 or exposed to soluble R. equi antigen lysed R. equi-infected target cells.

32 Like mycobacteria, R. equi is phagocytosed by alveolar macrophages and repl

33 al growth system was developed for obtaining R. equi CFS antigens.

34 irulence plasmid by an avirulent ancestor of R. equi, coevolution between the plasmid and the chromos

35 We present two HIV-associated cases of R. equi infection from Vietnam and discuss the unique di

36 developed will allow the characterization of R. equi virulence mechanisms and the creation of other a

37 fic CD4+ Th1 cells could effect clearance of R. equi from the lung.

38 Adoptive transfer of a clearance of R. equi from the lungs.

39 Pulmonary clearance of R. equi requires functional CD4+ T cells and gamma inter

40 sufficient to effect pulmonary clearance of R. equi.

41 uction of the characteristic salmon color of R. equi.

42 ificantly increased tissue concentrations of R. equi.

43 ally replicating plasmid for construction of R. equi mutants.

44 ined that the major virulence determinant of R. equi is the surface bound virulence associated protei

45 ture techniques or serology for diagnosis of R. equi pneumonia in foals.

46 more sensitive and specific for diagnosis of R. equi pneumonia than are other available diagnostic te

47 itrite mediates the intracellular killing of R. equi by IFN-gamma-activated macrophages.

48 not necessary for recognition and killing of R. equi-infected cells.

49 Killing of R. equi-infected macrophages by effector cells was equal

50 with CTL obtained from the blood, killing of R. equi-infected targets by pulmonary effectors was not

51 regulated in macrophages and in the lungs of R. equi-infected foals, we hypothesized that vapG could

52 presence of VapA inhibits the maturation of R. equi-containing phagosomes and promotes intracellular

53 ts the predominantly opportunistic nature of R. equi infection in this host and a zoonotic origin.

54 hat recognized the vapA virulence plasmid of R. equi had a diagnostic sensitivity of 100% and specifi

55 uld be extremely useful in the prevention of R. equi disease in horses.

56 ansferred from plasmid-containing strains of R. equi (donor) to plasmid-free R. equi strains (recipie

57 Virulent strains of R. equi bear a large plasmid that is required for intrac

58 All strains of R. equi isolated from foals and approximately a third is

59 and between traA(+)/vapAB(-)--a new type of R. equi plasmid--and cattle.

60 proof of a role for vapA in the virulence of R. equi, and demonstrate that its presence is essential

61 Inflammatory cells from either L. major- or R. equi-infected C57BL/6 mice were sensitive to TNF-indu

62 Loss of pVAPN rendered R. equi avirulent in macrophages and mice.

63 e two proteins are not expressed by the same R. equi isolate.

64 infected with R. equi or exposed to soluble R. equi antigen lysed R. equi-infected target cells.

65 mmune adult horses and provide evidence that R. equi CFS proteins are antigen targets in the immunopr

66 In this study, the hypothesis that R. equi-specific cytotoxic T lymphocytes (CTL) are prese

67 and VapE, which are encoded by genes on the R. equi virulence plasmid.

68 nd alveolar macrophages, suggesting that the R. equi-specific, major histocompatibility complex-unres

69 8+ CTL, which may play a role in immunity to R. equi.

70 rophages were fully capable of responding to R. equi infection, and because RAW-264 cells transfected

71 oduced virtually no cytokines in response to R. equi infection, implicating a TLR pathway.

72 e exhibited diminished cytokine responses to R. equi.

73 bited markedly reduced cytokine responses to R. equi.

74 macrophage replication defect of a wild type R. equi strain lacking the vapA gene and enhances the pe

75 Unlike wild-type R. equi which replicates intracellularly, both of the mu

76 tudies showed that, in contrast to wild-type R. equi, the riboflavin-requiring mutant is attenuated b

77 h equine (pVAPA) and porcine (pVAPB variant) R. equi isolates.

78 cteria to ONOO(-) efficiently kills virulent R. equi.

79 e adult horses were challenged with virulent R. equi, and cells from the bronchoalveolar lavage fluid

80 r ability to clear a challenge with virulent R. equi.

81 e with VapA; the proteins are expressed when R. equi is cultured at 37 degrees C but not at 30 degree

82 ose of this study was to investigate whether R. equi-specific CD4+ Th1 cells could effect clearance o

83 Our findings support a model in which R. equi virulence is conferred by host-adapted plasmids.

84 equi isolated from young horses (foals) with R. equi pneumonia, carry an 80-90 kb virulence plasmid a

85 ntigen-presenting cells either infected with R. equi or exposed to soluble R. equi antigen lysed R. e

86 stimulation of pulmonary T-lymphocytes with R. equi CFS resulted in significant proliferation and a

87 ek after experimental infection of mice with R. equi resulted in more severe disease and significantl

88 ived pulmonary T lymphocytes stimulated with R. equi lysed infected alveolar macrophages and peripher