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1  G (IgG) antibodies reactive with Rickettsia rickettsii.
2 cavenger, inhibited the HO-1 induction by R. rickettsii.
3 fected cells within 5 h after exposure to R. rickettsii.
4 vein endothelial cells (HUVEC) by Rickettsia rickettsii.
5  several other agents, especially Rickettsia rickettsii.
6 a canis, Bartonella henselae, and Rickettsia rickettsii.
7 bilical vein after infection with Rickettsia rickettsii.
8 a spp.; the other is specific for Rickettsia rickettsii.
9 otypes that may not belong to the species R. rickettsii.
10 he genetic differentiation of isolates of R. rickettsii.
11 the robust differentiation of isolates of R. rickettsii.
12 (R. sanguineus) implicated as a vector of R. rickettsii.
13 ing, tick-borne disease caused by Rickettsia rickettsii.
14 le only moderately inhibiting motility of R. rickettsii.
15 urred in 11 patients, including 1 against R. rickettsii, 4 against R. parkeri, and 6 against R. ambly
16 ovascular endothelial cells infected with R. rickettsii, a prototypical species known to cause Rocky
17 tructure and morphogenesis of the Rickettsia rickettsii actin tail relative to Shigella and Listeria
18  and compositional characteristics of the R. rickettsii actin tail suggest that rickettsial ABM is me
19 ells consequent to infection with Rickettsia rickettsii, an obligate intracellular gram-negative bact
20 l apoptosis was explored by using Rickettsia rickettsii, an obligate intracellular Gram-negative bact
21 elial cells during infection with Rickettsia rickettsii, an obligate, intracellular bacterium, and th
22    SQ-PCR is suitable for quantitation of R. rickettsii and 10 other genotypes of spotted fever group
23      By indirect immunofluorescence, both R. rickettsii and Listeria monocytogenes actin tails were s
24 e dynamics and behavior of ABM of Rickettsia rickettsii and Listeria monocytogenes.
25  the detection and enumeration of Rickettsia rickettsii and other closely related spotted fever group
26  enhance the clearance of infections with R. rickettsii and other intracellular pathogens with simila
27 ver and boutonneuse fever, due to Rickettsia rickettsii and R. conorii, respectively, are characteriz
28 uence analysis of insertion sites in both R. rickettsii and R. prowazekii indicated that insertions w
29 ween ELB and R. prowazekii and 25 between R. rickettsii and R. prowazekii; there were 30 base pair di
30                The cloned lepB genes from R. rickettsii and R. typhi have been demonstrated to posses
31 ce analysis of the cloned lepB genes from R. rickettsii and R. typhi shows open reading frames of 801
32  signal peptidase lepB genes from Rickettsia rickettsii and Rickettsia typhi, the etiologic agents of
33 ant associated with infection of HUVEC by R. rickettsii and that intracellular oxidant activity sensi
34 acted from Ehrlichia chaffeensis, Rickettsia rickettsii, and Bartonella henselae.
35  caused by Ehrlichia chaffeensis, Rickettsia rickettsii, and Coxiella burnetti, no significant cross-
36 , two presumptive cases of infection with R. rickettsii, and one presumptive case of infection with R
37 o identify it as a distinct subspecies of R. rickettsii, and propose the name Rickettsia rickettsii s
38 e, we compared ELB, Rickettsia australis, R. rickettsii, and R. akari with the louse-borne R. prowaze
39 esidents and that serologic testing using R. rickettsii antigen may miss cases of spotted fever ricke
40 nselae, one to E. chaffeensis, and one to R. rickettsii antigen; however, none had clinical or hemato
41 vinsonii, and 22 seroconverted to Rickettsia rickettsii antigens.
42 s suggest that species of SFGR other than R. rickettsii are associated with illness among North Carol
43 oup rickettsiae (SFGR) other than Rickettsia rickettsii are responsible for spotted fever rickettsios
44 G or IgM antibodies reactive with Rickettsia rickettsii at a diagnostic titer (i.e., >/=64); however,
45 emonstrated antibody titers reactive with R. rickettsii at titers >=64, whereas 6.3% of donors from O
46 ocytophilum, Ehrlichia canis, and Rickettsia rickettsii), but the sample was highly positive for B. w
47 ed to be necessary, since inactivation of R. rickettsii by heat or formalin fixation, or incubation o
48   As few as 5 copies of the rOmpA gene of R. rickettsii can be detected.
49 lvement was supported by the finding that R. rickettsii can induce NF-kappaB activation in cytoplasmi
50  reference human antisera against Rickettsia rickettsii, Chlamydia group positive, Treponema pallidum
51 rtain pathogenic organisms (e.g., Rickettsia rickettsii), data documenting endothelial cell apoptosis
52                                Strains of R. rickettsii differ dramatically in virulence.
53                       The SFG rickettsia, R. rickettsii, displayed long actin tails (>10 micrometer)
54                                           R. rickettsii DNA was detected in nonengorged R. sanguineus
55 nsis, Orientia tsutsugamushi, and Rickettsia rickettsii, etc.
56 cytogenes, Shigella flexneri, and Rickettsia rickettsii, exploit the host cytoskeleton by using actin
57 ovascular endothelial cells infected with R. rickettsii for 24 or 48 h were challenged with staurospo
58 oteins in actin-based motility of Rickettsia rickettsii have not been established.
59 two other nonpathogenic isolates (Rickettsia rickettsii Hip2 and Rickettsia montana M5/6) with respec
60 rucella canis IFA-positive and 10 Rickettsia rickettsii IFA-positive dogs.
61 s concern about its potential to transmit R. rickettsii in other settings.
62  the role of A. cooperi in the ecology of R. rickettsii in the area studied, but they add two more sp
63                   Infection of cells with R. rickettsii in the presence of BM-1 (50 nM) did not signi
64 ished genome sequences of R. sibirica and R. rickettsii, indicating that this region is a hot spot fo
65                             However, when R. rickettsii-induced activation of NF-kappa B was inhibite
66                                           R. rickettsii-induced activation of NF-kappaB may be an imp
67                 In this study, we explore R. rickettsii-induced activation of the nuclear factor-kapp
68                                           R. rickettsii-induced COX-2 was sensitive to inhibitors of
69                                           R. rickettsii-induced expression of cIAP2 in host endotheli
70 sis inhibitor cycloheximide did not block R. rickettsii-induced increase in TF mRNA levels and actual
71  involvement of classical PKC pathways in R. rickettsii-induced NF-kappaB activation but the possible
72 stream signaling event in the pathway for R. rickettsii-induced NF-kappaB activation.
73  of the transcription factor NF-kappaB in R. rickettsii-induced TF expression was demonstrated by usi
74 oxides can be detected in supernatants of R. rickettsii-infected cells shortly after rickettsial expo
75  disease similar to that of nonvaccinated R. rickettsii-infected dogs.
76 th immunoprecipitates from uninfected and R. rickettsii-infected ECs, revealed significant increases
77      Here, we investigate whether Rickettsia rickettsii-infected host endothelial cells resist the ef
78 ception of two of four serum samples from R. rickettsii-infected patients that were reactive by IFA o
79  work in our laboratory demonstrated that R. rickettsii infection activates the transcription factor
80 in conferring protection against virulent R. rickettsii infection challenge in a newly established ca
81 with relatively similar susceptibility to R. rickettsii infection in vitro but considerable variation
82                                           R. rickettsii infection induces a biphasic pattern of the n
83                The findings indicate that R. rickettsii infection induces HO-1 expression in host end
84                                      Since R rickettsii infection induces thrombotic vascular occlusi
85                                   Rickettsia rickettsii infection of endothelial cells is manifested
86 tutive HO isozymes, HO-1 and HO-2, during R. rickettsii infection of endothelial cells.
87 emokines and prostaglandins after Rickettsia rickettsii infection of human cerebral, dermal, and pulm
88 ls of infection, we demonstrate here that R. rickettsii infection of human EC causes robust induction
89          In this study, it was shown that R. rickettsii infection of human umbilical vein endothelial
90                                   Rickettsia rickettsii infection results in numerous responses by cu
91              This study demonstrates that R. rickettsii infection results in transcriptional activati
92 ility to secrete prostaglandin E(2) after R. rickettsii infection.
93 o differentiate 36 historical isolates of R. rickettsii into three different phylogenetic clades cont
94 mparison of the two genomes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a h
95 ur differences in gene expression between R. rickettsii Iowa and R. rickettsii strain R.
96  R strains were compared to the avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith
97                                  Although R. rickettsii Iowa does not cause apparent disease, infecti
98                                           R. rickettsii Iowa is avirulent in a guinea pig model of in
99                              In addition, R. rickettsii Iowa is defective in the processing of rOmpB,
100        A whole-genome alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a
101                   One of the deletions in R. rickettsii Iowa truncates rompA, encoding a major surfac
102 ttsii, the genome of an avirulent strain, R. rickettsii Iowa, was sequenced and compared to the genom
103 tors that contribute to the avirulence of R. rickettsii Iowa.
104 cence confirmed the absence of rOmpA from R. rickettsii Iowa.
105                                   Rickettsia rickettsii is an obligate intracellular pathogen that is
106 alysis demonstrated that the lepB gene of R. rickettsii is cotranscribed in a polycistronic message w
107 ins, suggest that actin-based motility of R. rickettsii is independent of N-WASP and the Arp2/3 compl
108 kettsia species, including R. conorii and R. rickettsii, is acutely dependent on adherence to and inv
109 , a tick-borne zoonosis caused by Rickettsia rickettsii, is among the most lethal of all infectious d
110  obligate intracellular bacterium Rickettsia rickettsii, is associated with widespread infection of t
111  causative agent of this disease, Rickettsia rickettsii, is transmitted by several species of ticks,
112 nguineus ticks collected at one home, and R. rickettsii isolates were cultured from these ticks.
113 ovel NF-kappaB activation pathway wherein R. rickettsii may interact with and activate host cell tran
114                                           R. rickettsii Morgan and R strains were compared to the avi
115 sing cells) but only moderately inhibited R. rickettsii motility.
116 und suggest that the molecular ecology of R. rickettsii needs more investigation.
117 ressed N-WASP domains did not localize to R. rickettsii or their actin tails.
118  and to either Coxiella burnetii, Rickettsia rickettsii, or Rickettsia typhi was infrequent; however,
119 0 min, and was dependent on the number of R. rickettsii organisms added.
120 is of time-lapse images demonstrated that R. rickettsii organisms move through the cell cytoplasm at
121                                At 4 hours, R rickettsii organisms were clearly visible within approxi
122  in those endothelial cells that contained R rickettsii organisms.
123                                        In R. rickettsii R, the nonlytic plaque phenotype resulted fro
124                     A nonlytic variant of R. rickettsii R, which typically produces clear plaques, wa
125 anis, E. chaffeensis, E. ewingii, Rickettsia rickettsii, R. conorii, and other spotted fever group ri
126 bolic antioxidant, after inoculation with R. rickettsii restored the intracellular levels of thiols a
127                                   Rickettsia rickettsii, Rickettsia parkeri, and Rickettsia akari are
128 erologic reactivity of the paired sera to R. rickettsii, Rickettsia parkeri, and Rickettsia amblyommi
129                                              Rickettsii rickettsii, the etiologic agent of Rocky Moun
130 alignment comparing R. rickettsii Iowa to R. rickettsii Sheila Smith revealed a total of 143 deletion
131 omes revealed that R. rickettsii Iowa and R. rickettsii Sheila Smith share a high degree of sequence
132 avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith strains.
133 equent challenge with the virulent strain R. rickettsii Sheila Smith.
134 ared to the genome of the virulent strain R. rickettsii Sheila Smith.
135 aB activation requires cellular uptake of R. rickettsii, since treatment of EC with cytochalasin B du
136 expression between R. rickettsii Iowa and R. rickettsii strain R.
137  rickettsii, and propose the name Rickettsia rickettsii subsp californica subsp nov.
138 ed that the individual actin filaments of R. rickettsii tails are >1 micrometer long, arranged roughl
139  viability at 96 h after inoculation with R. rickettsii than did untreated infected cells.
140  miyamotoi, Borrelia mayonii, and Rickettsia rickettsii The sensitivity for identification of B. burg
141 potted fever group (SFG), such as Rickettsia rickettsii, the agent of Rocky Mountain spotted fever.
142                                   Rickettsia rickettsii, the causative agent of Rocky Mountain spotte
143 infection of endothelial cells by Rickettsia rickettsii, the causative agent of Rocky Mountain spotte
144  cooperi in the enzootic cycle of Rickettsia rickettsii, the etiologic agent of Brazilian spotted fev
145  primary target of infection with Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte
146                                   Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte
147 sia Rickettsia montanensis, a relative of R. rickettsii, the etiologic agent of Rocky Mountain spotte
148 y fatal human infection caused by Rickettsia rickettsii, the etiologic agent of Rocky Mountain spotte
149 o, but distinct from, isolates of Rickettsia rickettsii, the etiological agent of RMSF.
150 entify genes involved in the virulence of R. rickettsii, the genome of an avirulent strain, R. ricket
151 fy potential determinants of virulence in R. rickettsii, the genomes of two additional strains were s
152 s from two independent strains of Rickettsia rickettsii, the virulent R strain and the avirulent Iowa
153                                           R. rickettsii, therefore, appeared to inhibit host cell apo
154 lly expressed in HeLa cells infected with R. rickettsii to assess their effects on rickettsial motili
155 plished by addition of partially purified R. rickettsii to endothelial cell cytoplasmic extracts.
156 l cells, nor did it affect the ability of R. rickettsii to form lytic plaques in Vero cells.
157 ave used random transposon mutagenesis of R. rickettsii to generate a small-plaque mutant that is def
158 of intracellular rickettsiae demonstrated R. rickettsii to have polar associations of cytoskeletal ma
159                      In addition, Rickettsia rickettsii was detected by PCR/ESI-MS from four specimen
160 ariner-based transposon system in Rickettsia rickettsii were determined using a plaque assay system f
161       Infection of cultured human EC with R. rickettsii with simultaneous inhibition of NF-kappa B in

 
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