ライフサイエンスコーパス: rickettsii

1 fected cells within 5 h after exposure to R. rickettsii.

2 vein endothelial cells (HUVEC) by Rickettsia rickettsii.

3 several other agents, especially Rickettsia rickettsii.

4 a spp.; the other is specific for Rickettsia rickettsii.

5 a canis, Bartonella henselae, and Rickettsia rickettsii.

6 bilical vein after infection with Rickettsia rickettsii.

7 otypes that may not belong to the species R. rickettsii.

8 he genetic differentiation of isolates of R. rickettsii.

9 the robust differentiation of isolates of R. rickettsii.

10 (R. sanguineus) implicated as a vector of R. rickettsii.

11 ing, tick-borne disease caused by Rickettsia rickettsii.

12 le only moderately inhibiting motility of R. rickettsii.

13 cavenger, inhibited the HO-1 induction by R. rickettsii.

14 urred in 11 patients, including 1 against R. rickettsii, 4 against R. parkeri, and 6 against R. ambly

15 ovascular endothelial cells infected with R. rickettsii, a prototypical species known to cause Rocky

16 tructure and morphogenesis of the Rickettsia rickettsii actin tail relative to Shigella and Listeria

17 and compositional characteristics of the R. rickettsii actin tail suggest that rickettsial ABM is me

18 ells consequent to infection with Rickettsia rickettsii, an obligate intracellular gram-negative bact

19 l apoptosis was explored by using Rickettsia rickettsii, an obligate intracellular Gram-negative bact

20 elial cells during infection with Rickettsia rickettsii, an obligate, intracellular bacterium, and th

21 SQ-PCR is suitable for quantitation of R. rickettsii and 10 other genotypes of spotted fever group

22 By indirect immunofluorescence, both R. rickettsii and Listeria monocytogenes actin tails were s

23 e dynamics and behavior of ABM of Rickettsia rickettsii and Listeria monocytogenes.

24 the detection and enumeration of Rickettsia rickettsii and other closely related spotted fever group

25 enhance the clearance of infections with R. rickettsii and other intracellular pathogens with simila

26 ver and boutonneuse fever, due to Rickettsia rickettsii and R. conorii, respectively, are characteriz

27 uence analysis of insertion sites in both R. rickettsii and R. prowazekii indicated that insertions w

28 ween ELB and R. prowazekii and 25 between R. rickettsii and R. prowazekii; there were 30 base pair di

29 The cloned lepB genes from R. rickettsii and R. typhi have been demonstrated to posses

30 ce analysis of the cloned lepB genes from R. rickettsii and R. typhi shows open reading frames of 801

31 signal peptidase lepB genes from Rickettsia rickettsii and Rickettsia typhi, the etiologic agents of

32 ant associated with infection of HUVEC by R. rickettsii and that intracellular oxidant activity sensi

33 acted from Ehrlichia chaffeensis, Rickettsia rickettsii, and Bartonella henselae.

34 caused by Ehrlichia chaffeensis, Rickettsia rickettsii, and Coxiella burnetti, no significant cross-

35 , two presumptive cases of infection with R. rickettsii, and one presumptive case of infection with R

36 e, we compared ELB, Rickettsia australis, R. rickettsii, and R. akari with the louse-borne R. prowaze

37 esidents and that serologic testing using R. rickettsii antigen may miss cases of spotted fever ricke

38 nselae, one to E. chaffeensis, and one to R. rickettsii antigen; however, none had clinical or hemato

39 vinsonii, and 22 seroconverted to Rickettsia rickettsii antigens.

40 s suggest that species of SFGR other than R. rickettsii are associated with illness among North Carol

41 oup rickettsiae (SFGR) other than Rickettsia rickettsii are responsible for spotted fever rickettsios

42 G or IgM antibodies reactive with Rickettsia rickettsii at a diagnostic titer (i.e., >/=64); however,

43 ocytophilum, Ehrlichia canis, and Rickettsia rickettsii), but the sample was highly positive for B. w

44 ed to be necessary, since inactivation of R. rickettsii by heat or formalin fixation, or incubation o

45 As few as 5 copies of the rOmpA gene of R. rickettsii can be detected.

46 lvement was supported by the finding that R. rickettsii can induce NF-kappaB activation in cytoplasmi

47 reference human antisera against Rickettsia rickettsii, Chlamydia group positive, Treponema pallidum

48 rtain pathogenic organisms (e.g., Rickettsia rickettsii), data documenting endothelial cell apoptosis

49 Strains of R. rickettsii differ dramatically in virulence.

50 The SFG rickettsia, R. rickettsii, displayed long actin tails (>10 micrometer)

51 R. rickettsii DNA was detected in nonengorged R. sanguineus

52 cytogenes, Shigella flexneri, and Rickettsia rickettsii, exploit the host cytoskeleton by using actin

53 ovascular endothelial cells infected with R. rickettsii for 24 or 48 h were challenged with staurospo

54 oteins in actin-based motility of Rickettsia rickettsii have not been established.

55 two other nonpathogenic isolates (Rickettsia rickettsii Hip2 and Rickettsia montana M5/6) with respec

56 s concern about its potential to transmit R. rickettsii in other settings.

57 the role of A. cooperi in the ecology of R. rickettsii in the area studied, but they add two more sp

58 Infection of cells with R. rickettsii in the presence of BM-1 (50 nM) did not signi

59 ished genome sequences of R. sibirica and R. rickettsii, indicating that this region is a hot spot fo

60 However, when R. rickettsii-induced activation of NF-kappa B was inhibite

61 R. rickettsii-induced activation of NF-kappaB may be an imp

62 In this study, we explore R. rickettsii-induced activation of the nuclear factor-kapp

63 R. rickettsii-induced COX-2 was sensitive to inhibitors of

64 R. rickettsii-induced expression of cIAP2 in host endotheli

65 sis inhibitor cycloheximide did not block R. rickettsii-induced increase in TF mRNA levels and actual

66 involvement of classical PKC pathways in R. rickettsii-induced NF-kappaB activation but the possible

67 stream signaling event in the pathway for R. rickettsii-induced NF-kappaB activation.

68 of the transcription factor NF-kappaB in R. rickettsii-induced TF expression was demonstrated by usi

69 oxides can be detected in supernatants of R. rickettsii-infected cells shortly after rickettsial expo

70 th immunoprecipitates from uninfected and R. rickettsii-infected ECs, revealed significant increases

71 Here, we investigate whether Rickettsia rickettsii-infected host endothelial cells resist the ef

72 ception of two of four serum samples from R. rickettsii-infected patients that were reactive by IFA o

73 work in our laboratory demonstrated that R. rickettsii infection activates the transcription factor

74 with relatively similar susceptibility to R. rickettsii infection in vitro but considerable variation

75 R. rickettsii infection induces a biphasic pattern of the n

76 The findings indicate that R. rickettsii infection induces HO-1 expression in host end

77 Since R rickettsii infection induces thrombotic vascular occlusi

78 Rickettsia rickettsii infection of endothelial cells is manifested

79 tutive HO isozymes, HO-1 and HO-2, during R. rickettsii infection of endothelial cells.

80 emokines and prostaglandins after Rickettsia rickettsii infection of human cerebral, dermal, and pulm

81 ls of infection, we demonstrate here that R. rickettsii infection of human EC causes robust induction

82 In this study, it was shown that R. rickettsii infection of human umbilical vein endothelial

83 Rickettsia rickettsii infection results in numerous responses by cu

84 This study demonstrates that R. rickettsii infection results in transcriptional activati

85 ility to secrete prostaglandin E(2) after R. rickettsii infection.

86 o differentiate 36 historical isolates of R. rickettsii into three different phylogenetic clades cont

87 mparison of the two genomes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a h

88 ur differences in gene expression between R. rickettsii Iowa and R. rickettsii strain R.

89 R strains were compared to the avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith

90 Although R. rickettsii Iowa does not cause apparent disease, infecti

91 R. rickettsii Iowa is avirulent in a guinea pig model of in

92 In addition, R. rickettsii Iowa is defective in the processing of rOmpB,

93 A whole-genome alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a

94 One of the deletions in R. rickettsii Iowa truncates rompA, encoding a major surfac

95 ttsii, the genome of an avirulent strain, R. rickettsii Iowa, was sequenced and compared to the genom

96 tors that contribute to the avirulence of R. rickettsii Iowa.

97 cence confirmed the absence of rOmpA from R. rickettsii Iowa.

98 Rickettsia rickettsii is an obligate intracellular pathogen that is

99 Rickettsia rickettsii is an obligate intracellular pathogen that is

100 alysis demonstrated that the lepB gene of R. rickettsii is cotranscribed in a polycistronic message w

101 ins, suggest that actin-based motility of R. rickettsii is independent of N-WASP and the Arp2/3 compl

102 kettsia species, including R. conorii and R. rickettsii, is acutely dependent on adherence to and inv

103 , a tick-borne zoonosis caused by Rickettsia rickettsii, is among the most lethal of all infectious d

104 obligate intracellular bacterium Rickettsia rickettsii, is associated with widespread infection of t

105 nguineus ticks collected at one home, and R. rickettsii isolates were cultured from these ticks.

106 ovel NF-kappaB activation pathway wherein R. rickettsii may interact with and activate host cell tran

107 R. rickettsii Morgan and R strains were compared to the avi

108 sing cells) but only moderately inhibited R. rickettsii motility.

109 und suggest that the molecular ecology of R. rickettsii needs more investigation.

110 ressed N-WASP domains did not localize to R. rickettsii or their actin tails.

111 and to either Coxiella burnetii, Rickettsia rickettsii, or Rickettsia typhi was infrequent; however,

112 0 min, and was dependent on the number of R. rickettsii organisms added.

113 is of time-lapse images demonstrated that R. rickettsii organisms move through the cell cytoplasm at

114 At 4 hours, R rickettsii organisms were clearly visible within approxi

115 in those endothelial cells that contained R rickettsii organisms.

116 In R. rickettsii R, the nonlytic plaque phenotype resulted fro

117 A nonlytic variant of R. rickettsii R, which typically produces clear plaques, wa

118 anis, E. chaffeensis, E. ewingii, Rickettsia rickettsii, R. conorii, and other spotted fever group ri

119 bolic antioxidant, after inoculation with R. rickettsii restored the intracellular levels of thiols a

120 Rickettsia rickettsii, Rickettsia parkeri, and Rickettsia akari are

121 erologic reactivity of the paired sera to R. rickettsii, Rickettsia parkeri, and Rickettsia amblyommi

122 Rickettsii rickettsii, the etiologic agent of Rocky Moun

123 alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a total of 143 deletion

124 omes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a high degree of sequence

125 avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith strains.

126 equent challenge with the virulent strain R. rickettsii Sheila Smith.

127 ared to the genome of the virulent strain R. rickettsii Sheila Smith.

128 aB activation requires cellular uptake of R. rickettsii, since treatment of EC with cytochalasin B du

129 expression between R. rickettsii Iowa and R. rickettsii strain R.

130 ed that the individual actin filaments of R. rickettsii tails are >1 micrometer long, arranged roughl

131 viability at 96 h after inoculation with R. rickettsii than did untreated infected cells.

132 potted fever group (SFG), such as Rickettsia rickettsii, the agent of Rocky Mountain spotted fever.

133 Rickettsia rickettsii, the causative agent of Rocky Mountain spotte

134 infection of endothelial cells by Rickettsia rickettsii, the causative agent of Rocky Mountain spotte

135 cooperi in the enzootic cycle of Rickettsia rickettsii, the etiologic agent of Brazilian spotted fev

136 primary target of infection with Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte

137 Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte

138 sia Rickettsia montanensis, a relative of R. rickettsii, the etiologic agent of Rocky Mountain spotte

139 y fatal human infection caused by Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte

140 entify genes involved in the virulence of R. rickettsii, the genome of an avirulent strain, R. ricket

141 fy potential determinants of virulence in R. rickettsii, the genomes of two additional strains were s

142 s from two independent strains of Rickettsia rickettsii, the virulent R strain and the avirulent Iowa

143 R. rickettsii, therefore, appeared to inhibit host cell apo

144 lly expressed in HeLa cells infected with R. rickettsii to assess their effects on rickettsial motili

145 plished by addition of partially purified R. rickettsii to endothelial cell cytoplasmic extracts.

146 l cells, nor did it affect the ability of R. rickettsii to form lytic plaques in Vero cells.

147 ave used random transposon mutagenesis of R. rickettsii to generate a small-plaque mutant that is def

148 of intracellular rickettsiae demonstrated R. rickettsii to have polar associations of cytoskeletal ma

149 In addition, Rickettsia rickettsii was detected by PCR/ESI-MS from four specimen

150 ariner-based transposon system in Rickettsia rickettsii were determined using a plaque assay system f

151 Infection of cultured human EC with R. rickettsii with simultaneous inhibition of NF-kappa B in