ライフサイエンスコーパス: rickettsiae

1 tion tools have been successfully applied to rickettsiae.

2 e further genetic manipulation of pathogenic rickettsiae.

3 and that RANTES plays a role in immunity to rickettsiae.

4 nfections caused by A. marginale and related rickettsiae.

5 d nucleoside transport systems are absent in rickettsiae.

6 lular metabolism that only indirectly affect rickettsiae.

7 d not affect their ability to be infected by rickettsiae.

8 iffer significantly from those in the normal rickettsiae.

9 tects them from an ordinarily lethal dose of rickettsiae.

10 ic serological reactions of the typhus group rickettsiae.

11 facilitate genetic and biological studies of rickettsiae.

12 evelop shuttle vectors for transformation of rickettsiae.

13 stral to the virulent spotted fever group of rickettsiae.

14 nt species or strains of spotted fever group rickettsiae.

15 as is characteristic of spotted fever group rickettsiae.

16 i, R. conorii, and other spotted fever group rickettsiae.

17 are virulence factors of spotted fever group rickettsiae.

18 ing gene (ppcE) that is conserved only in TG rickettsiae.

19 ed as part of the tick's defense response to rickettsiae.

20 major surface antigen of spotted fever group rickettsiae.

21 dogenized or absent from spotted fever group rickettsiae.

22 induce actin-tail polymerization for the SFG rickettsiae.

23 i genome when compared to those of other SFG rickettsiae.

24 be involved in adhesion and virulence of the rickettsiae.

25 between spotted fever group and typhus group rickettsiae.

26 Fc receptor-mediated adherence of opsonized rickettsiae.

27 response system is still functional in these rickettsiae.

28 completely abolished by formalin fixation of rickettsiae.

29 human pathogen among the Spotted Fever Group rickettsiae.

30 e exhibited kinetics similar to that seen in rickettsiae.

31 d diseases are systemic infections caused by rickettsiae.

32 ri, R. australis, R. bellii, or typhus group rickettsiae.

33 nd other closely related spotted fever group rickettsiae.

34 rvoir for members of the spotted fever group rickettsiae.

35 erization of genetic analysis systems in the rickettsiae.

36 Rickettsiae, a diverse group of obligately intracellular

37 a potential target for enhanced clearance of rickettsiae and an effective strategy to reduce inflamma

38 c strategies of C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures d

39 participates in the interaction between SFG rickettsiae and host cells and suggests that in addition

40 tsioses, the interactions between pathogenic rickettsiae and microvascular endothelial cells remain p

41 epresent the antigens common to LPSs from TG rickettsiae and P. vulgaris OX19.

42 Cs is associated with protective immunity to rickettsiae and that generation of antigen-specific immu

43 s implied three evolutionary lineages of SFG rickettsiae and that WB-8-2 and MOAa were most closely r

44 e subsets in immunity to spotted fever group rickettsiae and the first demonstration that clearance o

45 cular mechanisms of the interactions between rickettsiae and their host cells has largely been hinder

46 rt the hypothesis of a stable coevolution of rickettsiae and their tick hosts.

47 ted potential host cells kills extracellular rickettsiae and thus prevents the rickettsiae from infec

48 e is found in the majority of pathogenic SFG rickettsiae and, due to its sequence conservation among

49 the causative agents of spotted fever group rickettsiae, and existing polymerase chain reaction (PCR

50 TLR) family are involved in host response to rickettsiae, and yet the mechanisms by which these TLRs

51 Furthermore, the rickettsiae apparently retained their capacity for intra

52 ates that only live and metabolically active rickettsiae are capable of infection and inducing host c

53 cules in the maintenance and transmission of rickettsiae are discussed.

54 lice and fleas), whereas spotted fever group rickettsiae are exclusively vectored by ticks.

55 Da surface protein antigens (SPAs) of typhus rickettsiae are highly immunogenic and have been shown t

56 Spotted fever group (SFG) rickettsiae are human pathogens that infect cells in the

57 Spotted fever group rickettsiae are known to produce distinct plaque phenoty

58 tionary model of intracellular pathogenesis, rickettsiae are notorious for their use of transport sys

59 Rickettsiae are obligate intracellular pathogens that in

60 rthropod vectors: for instance, typhus group rickettsiae are principally vectored by insects (i.e., l

61 Rickettsiae are responsible for some of the most devasta

62 Pathogenic rickettsiae are the causative agents of Rocky Mountain s

63 Rickettsiae are well known as intracellular pathogens of

64 underlying the pathogenesis and evolution of rickettsiae as well as its potential to be used in ricke

65 t CD8 T lymphocytes provide immunity against rickettsiae besides that provided by the secretion of IF

66 nd severe illness after inhalation make some rickettsiae bioterrorism threats.

67 nd 10 other genotypes of spotted fever group rickettsiae but not for R. akari, R. australis, R. belli

68 d RANTES, differed in their capacity to kill rickettsiae by a nitric oxide-dependent mechanism and in

69 nd -secreted chemokine) killed intracellular rickettsiae by a nitric oxide-dependent mechanism.

70 esence of Ehrlichia phagocytophila genogroup rickettsiae by using a nested PCR technique.

71 we show for the first time that transformed rickettsiae can be used for the detection of CD8(+) T ce

72 These data suggest that rickettsiae can target DCs to stimulate a protective typ

73 Spotted fever group rickettsiae cause life-threatening human infections worl

74 Spotted fever group rickettsiae cause potentially life-threatening infection

75 uating the infectious titers of typhus group rickettsiae, cloning single plaque isolates, and testing

76 Cells infected with viable rickettsiae consistently displayed significantly increas

77 LPSs from two species of TG rickettsiae contained glucose, 3-deoxy-D-manno-octuloson

78 reatment conditions, a significant number of rickettsiae could be detected microscopically.

79 canning electron microscopy of intracellular rickettsiae demonstrated R. rickettsii to have polar ass

80 6S rRNA precursors in the methionine-starved rickettsiae did not differ significantly from those in t

81 In contrast, rickettsiae did not transport cytidylribonucleotides.

82 Together, these data demonstrate that, while rickettsiae do not contain endotoxic lipopolysaccharide,

83 solic localization within endothelial cells, rickettsiae efficiently entered and localized in both ph

84 critical for Rickettsia typhi (typhus group rickettsiae) entry but pseudogenized or absent from spot

85 Rickettsiae exploit this intracellular environment by us

86 After 72 h, inhibited survival of rickettsiae exposed to polyclonal antibodies or monoclon

87 Last, adoptive transfer of rickettsiae-exposed, TLR4-stimulated DCs activated NK ce

88 t in vitro cultures are a valuable source of rickettsiae for basic research and for the development o

89 ration that clearance of spotted fever group rickettsiae from endothelial cells requires immune CD8 T

90 and it also decreased the recovery of viable rickettsiae from endothelial cells.

91 racellular rickettsiae and thus prevents the rickettsiae from infecting the cells.

92 as to the potential origin of pathogenic SFG rickettsiae from nonpathogenic tick symbionts, or vice v

93 ole of chemokines in the immune clearance of rickettsiae from the vasculature.

94 The known mite-associated bacteria, rickettsiae, fungi, Protozoa, viruses, and nematodes rep

95 At 3 h, the opsonized rickettsiae had been internalized.

96 metabolic or light-emitting functions, these rickettsiae have an essential role in the early developm

97 rOmpA and rOmpB of spotted fever group (SFG) rickettsiae have been identified as adhesion and invasio

98 control, demonstrating that the typhus group rickettsiae have the capability of synthesizing as well

99 The causative agents, rickettsiae, have been divided according to biological,

100 hown previously and show here are present in rickettsiae, have never been reported in free-living bac

101 ckettsial stock cultures, the replication of rickettsiae in cell culture, the recovery of rickettsial

102 r to or concomitantly with the appearance of rickettsiae in erythrocytes.

103 he prevalence of E. phagocytophila genogroup rickettsiae in ixodid ticks of California may be lower t

104 d resulted in decreased levels of infectious rickettsiae in the spleen and liver 24 and 48 h later.

105 ngly, we observed that DvKPI associates with rickettsiae in vitro as well as in the tick midgut.

106 the importance of TLR4 in early immunity to rickettsiae in vivo, particularly that conferred by TLR4

107 Typhus group rickettsiae, including Rickettsia prowazekii and R. typh

108 e preferred target cells for most pathogenic rickettsiae, infection of monocytes/macrophages may also

109 four independent origins (introductions) of rickettsiae into North America from different Old World

110 Transformation of rickettsiae is a recent accomplishment, but utility of t

111 complete schema of nucleotide metabolism in rickettsiae is presented that is based on a combination

112 virulence for many bacteria, but its role in rickettsiae is unknown.

113 that this protein is expressed and active in rickettsiae isolated from embryonated hen egg yolk sacs.

114 activity for endothelial cells infected with rickettsiae may involve complex changes in cellular meta

115 se of host protection against infection with rickettsiae, most likely via IFN-gamma production.

116 Although rickettsiae moved more slowly, the actin filaments compr

117 ligate intracellular, vector-borne bacteria, rickettsiae must adapt to both mammalian and arthropod h

118 The mycetomic rickettsiae of two parthenogenetic book lice species are

119 cations for plaque formation of typhus group rickettsiae on the continuous fibroblast cell line Vero7

120 ment), previously identified in scrub typhus rickettsiae (Orientia tsutsugamushi) genomes, is present

121 However, several strains of the typhus group rickettsiae possess metK genes lacking obvious mutations

122 Typhus group rickettsiae (R. typhi and R. prowazekii) adhere to and l

123 veals extreme gene loss in typhus group (TG) rickettsiae relative to the levels for other rickettsial

124 actin tail associated with intracytoplasmic rickettsiae remained stationary in the cytoplasm as the

125 f toll-like receptor 4 (TLR4) in immunity to rickettsiae remains elusive.

126 The existence of intracellular rickettsiae requires entry, survival, and replication in

127 oteins and the major surface proteins of the rickettsiae revealed that these proteins are divided int

128 rides (LPSs) isolated from typhus group (TG) rickettsiae Rickettsia typhi and Rickettsia prowazekii w

129 nfected Vero cells revealed the typhus group rickettsiae, Rickettsia prowazekii and Rickettsia typhi,

130 cluding eight species of spotted fever group rickettsiae, seven species in the family Anaplasmataceae

131 c evidence suggests that spotted fever group rickettsiae (SFGR) other than Rickettsia rickettsii are

132 These rickettsiae show an evolutionary transition from a solit

133 Transfer of rickettsiae-stimulated DCs protected mice from lethal ri

134 bited by native folded SPA but not by intact rickettsiae, suggesting that they were on the SPA surfac

135 tsia typhi interactions and to determine how rickettsiae survive within phagocytic cells.

136 eal an important role for DCs in recognizing rickettsiae through TLR4 and inducing early antiricketts

137 solates, and testing the susceptibilities of rickettsiae to antibiotics.

138 sufficiently genetically distinct from other rickettsiae to be designated a new species, Rickettsia f

139 ea studied, but they add two more species of rickettsiae to the poorly developed list of species occu

140 In contrast, actin tails of rickettsiae trapped within the nucleus displayed dramati

141 The influx of AdoMet into rickettsiae was a saturable process with a K(T) of 2.3 m

142 Stable transformation of diverse rickettsiae was achieved with a shuttle vector system ba

143 Metabolic activity of rickettsiae was essential for the IFN-beta-mediated resp

144 sicidal activity of macrophages by opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, s

145 al rickettsicidal activity against opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, s

146 is, Babesia gibsonii, or spotted fever group rickettsiae, was obtained for seven dogs.

147 lity of nitric oxide (NO) to damage isolated rickettsiae were investigated.

148 , and in the presence of rifampin, resistant rickettsiae were selected.

149 The rickettsiae were subsequently grown in Vero cells, and c

150 the presence of an AdoMet transporter in the rickettsiae which, to our knowledge, is the first bacter

151 his is the first report of transformation of rickettsiae with a nonrickettsial (GFPUV) gene.

152 st characterized the in vitro interaction of rickettsiae with bone marrow-derived DCs (BMDCs) from re

153 Incubation of isolated rickettsiae with NO inhibited their ability to infect L9

154 th pRAM18/Rif/GFPuv yielded GFPuv-expressing rickettsiae within 2 weeks.

155 amily were identified in the closely related rickettsiae: wsp from Wolbachia sp., p44 from the agent