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 isolates-including MDR ones-were generally susce

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

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

5 R. equi/hoagii, R. corynebacterioides, and R. erythropol

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

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

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

9 goal was to passively immunize foals against R. equi by nebulizing mRNA encoding an equine monoclonal

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

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

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

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

14 he taxonomic and nomenclatural issues around R. equi in the light of recent phylogenomic evidence tha

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

16 ant differences in AST were observed between R. equi and non-equi species.

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

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

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

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

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

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

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

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

25 gns are used as means of controlling endemic R. equi infection on many farms.

26 perimentally infected with Rhodococcus equi (R. equi) and treated with MaR selected for MaR-resistant

27 severity and duration of pneumonia following R. equi infection.

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

29 from soil samples from 100 farms endemic for R. equi infections in Kentucky.

30 in appropriate empiric treatment options for R. equi.

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

32 Standard treatment for R. equi disease is dual-antimicrobial therapy with a mac

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

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

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

36 vel erm(51)-encoding resistance to MLS(B) in R. equi isolates from soil of horse-breeding farms.

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

38 at MaR use promotes multi-drug resistance in R. equi and commensals that are shed into their environm

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

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

41 rogramming innate immune responses, inducing R. equi-specific adaptive humoral and cell-mediated immu

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

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

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

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

46 two cases suggest the emergence of novel MDR R. equi strains.

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

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

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

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

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

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

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

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

55 sufficient to effect pulmonary clearance of R. equi.

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

57 nes in neutrophils, higher concentrations of R. equi-specific IgG(1) and IgG(4/7), and a higher numbe

58 ificantly increased tissue concentrations of R. equi.

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

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

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

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

63 sociated epidemiologically with emergence of R. equi resistant to MaR.

64 laboratory demonstrated decreased fitness of R. equi strains that were resistant to macrolides, rifam

65 Foals were immunized twice via gavage of R. equi (immunized group) or saline (control group) at a

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

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

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

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

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

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

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

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

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

75 n resistance on intracellular replication of R. equi in equine pulmonary macrophages and in an in viv

76 The SD of R. equi, Nocardia sp., M. nonchromogenicum, M. monacense

77 gens and reduce the duration and severity of R. equi pneumonia.

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

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

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

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

82 Progress in the molecular understanding of R. equi and its recent rise as a novel paradigm of multi

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

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

85 Best known as a horse pathogen, R. equi is commonly isolated from other animal species,

86 The standard for preventing R. equi pneumonia in foals is transfusion of hyperimmune

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

88 ction of susceptible and macrolide-resistant R. equi strains from equine clinical cases using a panel

89 treated with MaR selected for MaR-resistant R. equi, whereas MaR-susceptible R. equi out-competed re

90 cidence of macrolide- and rifampin-resistant R. equi isolates has been documented.

91 As typical in the rhodococci, R. equi niche specialization is extrachromosomally deter

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

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

94 R-resistant R. equi, whereas MaR-susceptible R. equi out-competed resistant isolates in GaM-treated o

95 the absence of antibiotics, the susceptible R. equi isolate outcompeted the macrolide- or rifampin-r

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

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

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

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

100 are with 10 cases diagnosed (majority due to R. equi) and managed.

101 ur data indicate that early life exposure to R. equi in the gastrointestinal tract can modulate innat

102 8+ CTL, which may play a role in immunity to R. equi.

103 antly more favorable AST profile relative to R. equi.

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

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

106 N-gamma producing lymphocytes in response to R. equi stimulation indicating T helper type 1 response

107 e exhibited diminished cytokine responses to R. equi.

108 bited markedly reduced cytokine responses to R. equi.

109 iotics are the standard of care for treating R. equi pneumonia in foals, and adjunctive therapies are

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

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

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

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

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

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

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

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

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

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

120 al foals after intrabronchial challenge with R. equi.

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

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

123 lar macrophages after ex vivo infection with R. equi.

124 foals were challenged intrabronchially with R. equi.

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

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

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