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1 ri, R. australis, R. bellii, or typhus group rickettsiae.
2 nd other closely related spotted fever group rickettsiae.
3 rvoir for members of the spotted fever group rickettsiae.
4 tion tools have been successfully applied to rickettsiae.
5 erization of genetic analysis systems in the rickettsiae.
6  and that RANTES plays a role in immunity to rickettsiae.
7 nfections caused by A. marginale and related rickettsiae.
8 d nucleoside transport systems are absent in rickettsiae.
9 lular metabolism that only indirectly affect rickettsiae.
10 d not affect their ability to be infected by rickettsiae.
11 iffer significantly from those in the normal rickettsiae.
12 ic serological reactions of the typhus group rickettsiae.
13 and VAPB were localized around intracellular rickettsiae.
14 s (ticks) permits successful transmission of rickettsiae.
15 dogenized or absent from spotted fever group rickettsiae.
16 e further genetic manipulation of pathogenic rickettsiae.
17 tects them from an ordinarily lethal dose of rickettsiae.
18 facilitate genetic and biological studies of rickettsiae.
19 evelop shuttle vectors for transformation of rickettsiae.
20 stral to the virulent spotted fever group of rickettsiae.
21 ever group rickettsiae, but not typhus group rickettsiae.
22 nt species or strains of spotted fever group rickettsiae.
23  as is characteristic of spotted fever group rickettsiae.
24 i, R. conorii, and other spotted fever group rickettsiae.
25 are virulence factors of spotted fever group rickettsiae.
26 ing gene (ppcE) that is conserved only in TG rickettsiae.
27 ed as part of the tick's defense response to rickettsiae.
28 major surface antigen of spotted fever group rickettsiae.
29 induce actin-tail polymerization for the SFG rickettsiae.
30 i genome when compared to those of other SFG rickettsiae.
31 be involved in adhesion and virulence of the rickettsiae.
32 between spotted fever group and typhus group rickettsiae.
33  Fc receptor-mediated adherence of opsonized rickettsiae.
34 response system is still functional in these rickettsiae.
35 completely abolished by formalin fixation of rickettsiae.
36 human pathogen among the Spotted Fever Group rickettsiae.
37 e exhibited kinetics similar to that seen in rickettsiae.
38 d diseases are systemic infections caused by rickettsiae.
39                                              Rickettsiae, a diverse group of obligately intracellular
40 infection with R. australis, suggesting that rickettsiae activate ASC inflammasome via a Toll-like re
41 crophages are one of the initial targets for rickettsiae after inoculation by ticks.
42 a potential target for enhanced clearance of rickettsiae and an effective strategy to reduce inflamma
43 c strategies of C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures d
44  participates in the interaction between SFG rickettsiae and host cells and suggests that in addition
45 tsioses, the interactions between pathogenic rickettsiae and microvascular endothelial cells remain p
46 epresent the antigens common to LPSs from TG rickettsiae and P. vulgaris OX19.
47 Cs is associated with protective immunity to rickettsiae and that generation of antigen-specific immu
48 s implied three evolutionary lineages of SFG rickettsiae and that WB-8-2 and MOAa were most closely r
49 l differences between tick- and insect-borne rickettsiae and the factors facilitating the incidence o
50 e subsets in immunity to spotted fever group rickettsiae and the first demonstration that clearance o
51 cular mechanisms of the interactions between rickettsiae and their host cells has largely been hinder
52 rt the hypothesis of a stable coevolution of rickettsiae and their tick hosts.
53   Uncovering the molecular interplay between rickettsiae and their vectors necessitates examining the
54 erstanding the intricate association between rickettsiae and their vectors.
55 ted potential host cells kills extracellular rickettsiae and thus prevents the rickettsiae from infec
56 e is found in the majority of pathogenic SFG rickettsiae and, due to its sequence conservation among
57  the causative agents of spotted fever group rickettsiae, and existing polymerase chain reaction (PCR
58 TLR) family are involved in host response to rickettsiae, and yet the mechanisms by which these TLRs
59                             Furthermore, the rickettsiae apparently retained their capacity for intra
60 ates that only live and metabolically active rickettsiae are capable of infection and inducing host c
61                                              Rickettsiae are cytosolically replicating, obligately in
62 cules in the maintenance and transmission of rickettsiae are discussed.
63 lice and fleas), whereas spotted fever group rickettsiae are exclusively vectored by ticks.
64 Da surface protein antigens (SPAs) of typhus rickettsiae are highly immunogenic and have been shown t
65                    Spotted fever group (SFG) rickettsiae are human pathogens that infect cells in the
66                          Spotted fever group rickettsiae are known to produce distinct plaque phenoty
67 tionary model of intracellular pathogenesis, rickettsiae are notorious for their use of transport sys
68                                              Rickettsiae are obligate intracellular pathogens that in
69 rthropod vectors: for instance, typhus group rickettsiae are principally vectored by insects (i.e., l
70                                              Rickettsiae are responsible for some of the most devasta
71                                   Pathogenic rickettsiae are the causative agents of Rocky Mountain s
72                                              Rickettsiae are well known as intracellular pathogens of
73 underlying the pathogenesis and evolution of rickettsiae as well as its potential to be used in ricke
74 t CD8 T lymphocytes provide immunity against rickettsiae besides that provided by the secretion of IF
75 nd severe illness after inhalation make some rickettsiae bioterrorism threats.
76 nd 10 other genotypes of spotted fever group rickettsiae but not for R. akari, R. australis, R. belli
77 d by many species of the spotted fever group rickettsiae, but not typhus group rickettsiae.
78 d RANTES, differed in their capacity to kill rickettsiae by a nitric oxide-dependent mechanism and in
79 nd -secreted chemokine) killed intracellular rickettsiae by a nitric oxide-dependent mechanism.
80 esence of Ehrlichia phagocytophila genogroup rickettsiae by using a nested PCR technique.
81  we show for the first time that transformed rickettsiae can be used for the detection of CD8(+) T ce
82                                              Rickettsiae can cause life-threatening infections in hum
83                      These data suggest that rickettsiae can target DCs to stimulate a protective typ
84                          Spotted fever group rickettsiae cause life-threatening human infections worl
85                          Spotted fever group rickettsiae cause potentially life-threatening infection
86 uating the infectious titers of typhus group rickettsiae, cloning single plaque isolates, and testing
87                   Cells infected with viable rickettsiae consistently displayed significantly increas
88                  LPSs from two species of TG rickettsiae contained glucose, 3-deoxy-D-manno-octuloson
89 reatment conditions, a significant number of rickettsiae could be detected microscopically.
90 canning electron microscopy of intracellular rickettsiae demonstrated R. rickettsii to have polar ass
91 6S rRNA precursors in the methionine-starved rickettsiae did not differ significantly from those in t
92                                 In contrast, rickettsiae did not transport cytidylribonucleotides.
93 Together, these data demonstrate that, while rickettsiae do not contain endotoxic lipopolysaccharide,
94 solic localization within endothelial cells, rickettsiae efficiently entered and localized in both ph
95  critical for Rickettsia typhi (typhus group rickettsiae) entry but pseudogenized or absent from spot
96                                              Rickettsiae exploit this intracellular environment by us
97            After 72 h, inhibited survival of rickettsiae exposed to polyclonal antibodies or monoclon
98                   Last, adoptive transfer of rickettsiae-exposed, TLR4-stimulated DCs activated NK ce
99 t in vitro cultures are a valuable source of rickettsiae for basic research and for the development o
100 ration that clearance of spotted fever group rickettsiae from endothelial cells requires immune CD8 T
101 and it also decreased the recovery of viable rickettsiae from endothelial cells.
102 racellular rickettsiae and thus prevents the rickettsiae from infecting the cells.
103 as to the potential origin of pathogenic SFG rickettsiae from nonpathogenic tick symbionts, or vice v
104 ole of chemokines in the immune clearance of rickettsiae from the vasculature.
105          The known mite-associated bacteria, rickettsiae, fungi, Protozoa, viruses, and nematodes rep
106                        At 3 h, the opsonized rickettsiae had been internalized.
107 metabolic or light-emitting functions, these rickettsiae have an essential role in the early developm
108 rOmpA and rOmpB of spotted fever group (SFG) rickettsiae have been identified as adhesion and invasio
109 control, demonstrating that the typhus group rickettsiae have the capability of synthesizing as well
110                        The causative agents, rickettsiae, have been divided according to biological,
111 hown previously and show here are present in rickettsiae, have never been reported in free-living bac
112 ckettsial stock cultures, the replication of rickettsiae in cell culture, the recovery of rickettsial
113 r to or concomitantly with the appearance of rickettsiae in erythrocytes.
114 he prevalence of E. phagocytophila genogroup rickettsiae in ixodid ticks of California may be lower t
115 lammasome and these molecules in controlling rickettsiae in macrophages.
116 d resulted in decreased levels of infectious rickettsiae in the spleen and liver 24 and 48 h later.
117 ve PCR (qPCR) assay was employed to quantify rickettsiae in tick salivary glands and saliva, as well
118 ngly, we observed that DvKPI associates with rickettsiae in vitro as well as in the tick midgut.
119  the importance of TLR4 in early immunity to rickettsiae in vivo, particularly that conferred by TLR4
120                                 Typhus group rickettsiae, including Rickettsia prowazekii and R. typh
121 e preferred target cells for most pathogenic rickettsiae, infection of monocytes/macrophages may also
122  four independent origins (introductions) of rickettsiae into North America from different Old World
123                            Transformation of rickettsiae is a recent accomplishment, but utility of t
124  complete schema of nucleotide metabolism in rickettsiae is presented that is based on a combination
125 virulence for many bacteria, but its role in rickettsiae is unknown.
126 that this protein is expressed and active in rickettsiae isolated from embryonated hen egg yolk sacs.
127 activity for endothelial cells infected with rickettsiae may involve complex changes in cellular meta
128 se of host protection against infection with rickettsiae, most likely via IFN-gamma production.
129                                     Although rickettsiae moved more slowly, the actin filaments compr
130 ligate intracellular, vector-borne bacteria, rickettsiae must adapt to both mammalian and arthropod h
131                                The mycetomic rickettsiae of two parthenogenetic book lice species are
132 cations for plaque formation of typhus group rickettsiae on the continuous fibroblast cell line Vero7
133 ment), previously identified in scrub typhus rickettsiae (Orientia tsutsugamushi) genomes, is present
134 However, several strains of the typhus group rickettsiae possess metK genes lacking obvious mutations
135                                 Typhus group rickettsiae (R. typhi and R. prowazekii) adhere to and l
136 veals extreme gene loss in typhus group (TG) rickettsiae relative to the levels for other rickettsial
137    However, it remains poorly understood how rickettsiae remain free in macrophages prior to establis
138  actin tail associated with intracytoplasmic rickettsiae remained stationary in the cytoplasm as the
139 f toll-like receptor 4 (TLR4) in immunity to rickettsiae remains elusive.
140               The existence of intracellular rickettsiae requires entry, survival, and replication in
141 oteins and the major surface proteins of the rickettsiae revealed that these proteins are divided int
142 rides (LPSs) isolated from typhus group (TG) rickettsiae Rickettsia typhi and Rickettsia prowazekii w
143 nfected Vero cells revealed the typhus group rickettsiae, Rickettsia prowazekii and Rickettsia typhi,
144 cluding eight species of spotted fever group rickettsiae, seven species in the family Anaplasmataceae
145 c evidence suggests that spotted fever group rickettsiae (SFGR) other than Rickettsia rickettsii are
146 ks were examined for the spotted fever group rickettsiae (SFGRs) using PCR and DNA sequencing of six
147                                        These rickettsiae show an evolutionary transition from a solit
148                                  Transfer of rickettsiae-stimulated DCs protected mice from lethal ri
149 bited by native folded SPA but not by intact rickettsiae, suggesting that they were on the SPA surfac
150 tsia typhi interactions and to determine how rickettsiae survive within phagocytic cells.
151 interkingdom ER contact uniquely mediated by rickettsiae that mimics some characteristics of traditio
152 eal an important role for DCs in recognizing rickettsiae through TLR4 and inducing early antiricketts
153 solates, and testing the susceptibilities of rickettsiae to antibiotics.
154 sufficiently genetically distinct from other rickettsiae to be designated a new species, Rickettsia f
155 ea studied, but they add two more species of rickettsiae to the poorly developed list of species occu
156                  In contrast, actin tails of rickettsiae trapped within the nucleus displayed dramati
157                    The influx of AdoMet into rickettsiae was a saturable process with a K(T) of 2.3 m
158             Stable transformation of diverse rickettsiae was achieved with a shuttle vector system ba
159                        Metabolic activity of rickettsiae was essential for the IFN-beta-mediated resp
160 sicidal activity of macrophages by opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, s
161 al rickettsicidal activity against opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, s
162 is, Babesia gibsonii, or spotted fever group rickettsiae, was obtained for seven dogs.
163 lity of nitric oxide (NO) to damage isolated rickettsiae were investigated.
164  R. parkeri than of "Ca Rickettsia andeanae" rickettsiae were present in tick saliva and salivary gla
165 , and in the presence of rifampin, resistant rickettsiae were selected.
166                                          The rickettsiae were subsequently grown in Vero cells, and c
167 the presence of an AdoMet transporter in the rickettsiae which, to our knowledge, is the first bacter
168 his is the first report of transformation of rickettsiae with a nonrickettsial (GFPUV) gene.
169 st characterized the in vitro interaction of rickettsiae with bone marrow-derived DCs (BMDCs) from re
170                       Incubation of isolated rickettsiae with NO inhibited their ability to infect L9
171 y insights into defining the interactions of rickettsiae with the host innate immune system.
172 th pRAM18/Rif/GFPuv yielded GFPuv-expressing rickettsiae within 2 weeks.
173 amily were identified in the closely related rickettsiae: wsp from Wolbachia sp., p44 from the agent

 
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