ライフサイエンスコーパス: R. rickettsii

1 R. rickettsii DNA was detected in nonengorged R. sanguin

2 R. rickettsii infection induces a biphasic pattern of th

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

4 R. rickettsii Morgan and R strains were compared to the

5 R. rickettsii, therefore, appeared to inhibit host cell

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

7 R. rickettsii-induced COX-2 was sensitive to inhibitors

8 R. rickettsii-induced expression of cIAP2 in host endoth

9 In addition, R. rickettsii Iowa is defective in the processing of rOm

10 nability to secrete prostaglandin E(2) after R. rickettsii infection.

11 occurred in 11 patients, including 1 against R. rickettsii, 4 against R. parkeri, and 6 against R. am

12 Although R. rickettsii Iowa does not cause apparent disease, infe

13 Rickettsia species, including R. conorii and R. rickettsii, is acutely dependent on adherence to and

14 sanguineus ticks collected at one home, and R. rickettsii isolates were cultured from these ticks.

15 genomes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a high degree of sequen

16 ne expression between R. rickettsii Iowa and R. rickettsii strain R.

17 ublished genome sequences of R. sibirica and R. rickettsii, indicating that this region is a hot spot

18 with immunoprecipitates from uninfected and R. rickettsii-infected ECs, revealed significant increas

19 gene, we compared ELB, Rickettsia australis, R. rickettsii, and R. akari with the louse-borne R. prow

20 and R strains were compared to the avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smi

21 between ELB and R. prowazekii and 25 between R. rickettsii and R. prowazekii; there were 30 base pair

22 four differences in gene expression between R. rickettsii Iowa and R. rickettsii strain R.

23 thesis inhibitor cycloheximide did not block R. rickettsii-induced increase in TF mRNA levels and act

24 By indirect immunofluorescence, both R. rickettsii and Listeria monocytogenes actin tails wer

25 Sequence analysis of insertion sites in both R. rickettsii and R. prowazekii indicated that insertion

26 xidant associated with infection of HUVEC by R. rickettsii and that intracellular oxidant activity se

27 t scavenger, inhibited the HO-1 induction by R. rickettsii.

28 A whole-genome alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith reveale

29 py of intracellular rickettsiae demonstrated R. rickettsii to have polar associations of cytoskeletal

30 stitutive HO isozymes, HO-1 and HO-2, during R. rickettsii infection of endothelial cells.

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

32 upstream signaling event in the pathway for R. rickettsii-induced NF-kappaB activation.

33 The cloned lepB genes from R. rickettsii and R. typhi have been demonstrated to pos

34 uence analysis of the cloned lepB genes from R. rickettsii and R. typhi shows open reading frames of

35 rescence confirmed the absence of rOmpA from R. rickettsii Iowa.

36 exception of two of four serum samples from R. rickettsii-infected patients that were reactive by IF

37 In R. rickettsii R, the nonlytic plaque phenotype resulted

38 One of the deletions in R. rickettsii Iowa truncates rompA, encoding a major sur

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

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

41 ntify potential determinants of virulence in R. rickettsii, the genomes of two additional strains wer

42 ressing cells) but only moderately inhibited R. rickettsii motility.

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

44 factors that contribute to the avirulence of R. rickettsii Iowa.

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

46 found suggest that the molecular ecology of R. rickettsii needs more investigation.

47 ealed that the individual actin filaments of R. rickettsii tails are >1 micrometer long, arranged rou

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

49 analysis demonstrated that the lepB gene of R. rickettsii is cotranscribed in a polycistronic messag

50 eared to be necessary, since inactivation of R. rickettsii by heat or formalin fixation, or incubatio

51 e to differentiate 36 historical isolates of R. rickettsii into three different phylogenetic clades c

52 r the genetic differentiation of isolates of R. rickettsii.

53 or the robust differentiation of isolates of R. rickettsii.

54 omains, suggest that actin-based motility of R. rickettsii is independent of N-WASP and the Arp2/3 co

55 while only moderately inhibiting motility of R. rickettsii.

56 e have used random transposon mutagenesis of R. rickettsii to generate a small-plaque mutant that is

57 t 60 min, and was dependent on the number of R. rickettsii organisms added.

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

59 ettsia Rickettsia montanensis, a relative of R. rickettsii, the etiologic agent of Rocky Mountain spo

60 Strains of R. rickettsii differ dramatically in virulence.

61 peroxides can be detected in supernatants of R. rickettsii-infected cells shortly after rickettsial e

62 appaB activation requires cellular uptake of R. rickettsii, since treatment of EC with cytochalasin B

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

64 ks (R. sanguineus) implicated as a vector of R. rickettsii.

65 identify genes involved in the virulence of R. rickettsii, the genome of an avirulent strain, R. ric

66 complished by addition of partially purified R. rickettsii to endothelial cell cytoplasmic extracts.

67 The SFG rickettsia, R. rickettsii, displayed long actin tails (>10 micromete

68 genotypes that may not belong to the species R. rickettsii.

69 ubsequent challenge with the virulent strain R. rickettsii Sheila Smith.

70 ompared to the genome of the virulent strain R. rickettsii Sheila Smith.

71 ckettsii, the genome of an avirulent strain, R. rickettsii Iowa, was sequenced and compared to the ge

72 ings suggest that species of SFGR other than R. rickettsii are associated with illness among North Ca

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

74 lysis of time-lapse images demonstrated that R. rickettsii organisms move through the cell cytoplasm

75 This study demonstrates that R. rickettsii infection results in transcriptional activ

76 nvolvement was supported by the finding that R. rickettsii can induce NF-kappaB activation in cytopla

77 odels of infection, we demonstrate here that R. rickettsii infection of human EC causes robust induct

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

79 Comparison of the two genomes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share

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

81 ral and compositional characteristics of the R. rickettsii actin tail suggest that rickettsial ABM is

82 infected cells within 5 h after exposure to R. rickettsii.

83 me alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a total of 143 delet

84 Expressed N-WASP domains did not localize to R. rickettsii or their actin tails.

85 henselae, one to E. chaffeensis, and one to R. rickettsii antigen; however, none had clinical or hem

86 e serologic reactivity of the paired sera to R. rickettsii, Rickettsia parkeri, and Rickettsia amblyo

87 ng with relatively similar susceptibility to R. rickettsii infection in vitro but considerable variat

88 ises concern about its potential to transmit R. rickettsii in other settings.

89 a residents and that serologic testing using R. rickettsii antigen may miss cases of spotted fever ri

90 he avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith strains.

91 However, when R. rickettsii-induced activation of NF-kappa B was inhib

92 y novel NF-kappaB activation pathway wherein R. rickettsii may interact with and activate host cell t

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

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

95 icrovascular endothelial cells infected with R. rickettsii for 24 or 48 h were challenged with stauro

96 ically expressed in HeLa cells infected with R. rickettsii to assess their effects on rickettsial mot

97 icrovascular endothelial cells infected with R. rickettsii, a prototypical species known to cause Roc

98 eri, two presumptive cases of infection with R. rickettsii, and one presumptive case of infection wit

99 to enhance the clearance of infections with R. rickettsii and other intracellular pathogens with sim

100 etabolic antioxidant, after inoculation with R. rickettsii restored the intracellular levels of thiol

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