ライフサイエンスコーパス: chlamydiae

1 f the missing bricks for the wall, exists in chlamydiae.

2 sglycosylation reactions occur in pathogenic Chlamydiae.

3 tion required live, transcriptionally active chlamydiae.

4 pholipase D (PLD) enzyme family varies among chlamydiae.

5 orate developmental regulation mechanisms in chlamydiae.

6 the site of attachment of surface-associated chlamydiae.

7 nsfer of genes between the rodent-associated Chlamydiae.

8 n of active disease were positive for ocular chlamydiae.

9 e 1 (Th1) response, which effectively clears chlamydiae.

10 nduced artificially with known quantities of chlamydiae.

11 n of the host ERK-cPLA2 signaling pathway by chlamydiae.

12 e of the cycle and in the infectious form of chlamydiae.

13 er infection, even in the presence of viable chlamydiae.

14 ndent on the size of the inoculating dose of chlamydiae.

15 centrations sufficient to kill intracellular chlamydiae.

16 d features related to the complex biology of chlamydiae.

17 t AHNAK is transiently recruited by invading chlamydiae.

18 ing that these genes are conserved among the chlamydiae.

19 osely homologous to those of hsp10s of other chlamydiae.

20 d were also less susceptible to infection by chlamydiae.

21 rescein-1, succinimidyl ester) conjugated to chlamydiae.

22 ectly examined the pH of vesicles containing chlamydiae.

23 t time the presence of PG in a member of the Chlamydiae.

24 ity to survive and are proficient killers of chlamydiae.

25 ce biochemical and physiological analyses of chlamydiae.

26 did not impact development of intracellular chlamydiae.

27 ired for optimal growth of the intracellular chlamydiae.

28 f multivesicular bodies to the intracellular chlamydiae.

29 ensis is a novel organism closely related to chlamydiae.

30 Chlamydiae, a diverse group of obligate intracellular pa

31 As obligate intracellular bacteria, chlamydiae actively modify their vacuole to exploit host

32 Modifying the ratio of phage to chlamydiae altered the course of infection and affected

33 e and characterized by decreased shedding of chlamydiae and an infection of shorter duration.

34 e shed approximately 3 logs fewer infectious chlamydiae and are protected from genital tract inflamma

35 is and C. pneumoniae MOMP exposure on intact chlamydiae and immunogenic properties might be because t

36 shown to inhibit intracellular infection by chlamydiae and mycobacteria in macrophages.

37 of the GT and may influence the clearance of chlamydiae and the development of tubal pathology.

38 dual deletion mutants were used to transform chlamydiae and the transformants were characterized phen

39 molecular and cellular interactions between chlamydiae and their host and large-scale prospective im

40 ry infection, shed high levels of infectious chlamydiae, and did not resolve the infection until 3 to

41 d spondyloarthritis continue to suggest that chlamydiae, and perhaps other pathogens function in the

42 karyotic cells that were similar to those of chlamydiae, and the microspheres were competitively inhi

43 have included numerous species of bacteria, chlamydiae, and viruses.

44 Chlamydiae appeared to exit the cell either (i) through

45 the response was dependent upon the dose of chlamydiae applied.

46 These pathobiotype differences among chlamydiae are also mirrored in their early interactions

47 Chlamydiae are bacterial parasites that carry out a dist

48 Overall, our findings show that chlamydiae are capable of the induction of interferon an

49 Chlamydiae are important pathogens and symbionts with un

50 s, reminiscent of effects seen in vitro when chlamydiae are incubated with gamma interferon.

51 Chlamydiae are intracellular bacteria that develop withi

52 nlike other intracellular bacteria, however, chlamydiae are metabolically inactive extracellularly an

53 Chlamydiae are obligate intracellular bacteria that enco

54 The chlamydiae are obligate intracellular bacteria that occu

55 Chlamydiae are obligate intracellular bacteria that repl

56 Chlamydiae are obligate intracellular bacteria that repl

57 Chlamydiae are obligate intracellular bacteria that repl

58 Chlamydiae are obligate intracellular bacterial pathogen

59 Chlamydiae are obligate intracellular bacterial pathogen

60 Chlamydiae are obligate intracellular bacterial pathogen

61 Chlamydiae are obligate intracellular bacterial pathogen

62 Chlamydiae are obligate intracellular gram-negative bact

63 The chlamydiae are obligate intracellular parasites that dev

64 Chlamydiae are obligate intracellular parasites which mu

65 Chlamydiae are obligate intracellular pathogens that can

66 Chlamydiae are obligate intracellular pathogens that eff

67 The chlamydiae are obligate intracellular pathogens that occ

68 The Chlamydiae are obligate intracellular pathogens that rep

69 Endocytosed chlamydiae are trafficked to the Golgi region and begin

70 Chlamydiae are widespread Gram-negative pathogens of hum

71 dritic cells (DC) pulsed ex vivo with killed chlamydiae as a novel approach to vaccination against ch

72 The enhanced production of this antigen by chlamydiae as a result of iron limitation is of particul

73 type III secretion systems of environmental chlamydiae at macromolecular resolution and find support

74 accompanied by dispersal of the chromatin as chlamydiae become transcriptionally active, although the

75 l cells, indicating that the MOMP and intact chlamydiae bind the same host receptor.

76 assays, IncA was detectable in intracellular chlamydiae but not within the inclusion membrane.

77 followed by conjunctival sampling to detect chlamydiae by commercial polymerase chain reaction.

78 nvestigated in the preferred target cells of chlamydiae, cervical epithelial cells, nor in vaginally

79 , as follows: Actinobacteria, Bacteroidetes, Chlamydiae, Chloroflexi, Euryarchaeota, Firmicutes, Fuso

80 Chlamydiae colonize the gastrointestinal tracts of both

81 Chlamydiae comprise important pathogenic and symbiotic b

82 rowth and late differentiation, suggest that chlamydiae contained in small non-fusogenic inclusions w

83 The survival of macrophage-adapted chlamydiae correlates with the multiplicity of infection

84 ports an evolutionary relationship among the chlamydiae, cyanobacteria, and plants and strengthens th

85 Discoveries that chlamydiae deploy an array of anti-host proteins have pl

86 or purify peptidoglycan (PG) from pathogenic Chlamydiae despite genetic and biochemical evidence and

87 Not all women infected with chlamydiae develop upper genital tract disease, but the

88 Chlamydiae dissociate themselves from the endocytic path

89 However, chlamydiae do not produce arginine, so they must import

90 Thus, chlamydiae do not reside within highly acidic vesicles a

91 Further, we show that strains of chlamydiae encoding the pzPLD, but not a strain lacking

92 ctions have been proposed as a means whereby chlamydiae evade immune resolution of infection.

93 is a safe niche for chlamydial replication, chlamydiae exploit a number of host cell processes, incl

94 Chlamydiae express a type III secretion system (T3SS) th

95 e three tests permit ready identification of chlamydiae for diagnostic and epidemiologic study.

96 titively inhibited the infectivity of viable chlamydiae for epithelial cells, indicating that the MOM

97 were also shown to reduce the infectivity of chlamydiae for epithelial cells.

98 l models has been the use of varied doses of chlamydiae for infection in different laboratories.

99 uctive chlamydial growth, thereby protecting chlamydiae from bactericidal attack.

100 tion, although very effective in eradicating chlamydiae from genital tissue and preventing upper geni

101 found that Th2-MoPn was unable to eradicate chlamydiae from the genital tract (GT) when it was trans

102 te that the immune system is unable to clear chlamydiae from the gut, so they can remain indefinitely

103 and late T3S inactivation upon detachment of chlamydiae from the inclusion membrane are crucial for c

104 ly NOS2(-/-) mice shed low numbers of viable chlamydiae from the lower genital tract after immunosupp

105 f the treatments affected shedding of viable chlamydiae from the lower urogenital tract, but the admi

106 posed to Desferal: (i) inclusions containing chlamydiae greatly delayed in maturation, (ii) substanti

107 Chlamydiae growing in target mucosal human epithelial ce

108 achomatis, to which a protein in extracts of chlamydiae harvested at 23 h after infection binds.

109 he existence of a peptidoglycan cell wall in chlamydiae has been debated for several years.

110 Fortunately, sexual transmission of chlamydiae has been described for the guinea pig model o

111 The existence of peptidoglycan (PG) in chlamydiae has long been debated.

112 It has been proposed that chlamydiae have a cytotoxic activity that contributes to

113 g dyes, here we show that some environmental chlamydiae have cell wall sacculi consisting of a novel

114 As obligate intracellular pathogens, chlamydiae have evolved sophisticated, yet undefined, me

115 in chlamydia-infected cells, suggesting that chlamydiae have evolved specific mechanisms for modifyin

116 s and recent advances that have revealed how chlamydiae have maintained conserved aspects of T3S whil

117 however efforts to purify PG from pathogenic Chlamydiae have remained unsuccessful.

118 The data presented here demonstrate that chlamydiae have the ability to convert a regulatory mole

119 We show here that chlamydiae have the ability to interfere with the NF-kap

120 Chlamydiae have to replicate within a cytoplasmic vacuol

121 For this purpose, chlamydiae hijack certain signaling pathways that preven

122 r set of host proteins as did endocytosis of chlamydiae; however, unlike viable chlamydial organisms,

123 atory infiltrate vs effective elimination of chlamydiae in a macrophage-dominated response.

124 he presence or absence of antibodies against chlamydiae in all sheep and bovine sera.

125 rom culture isolates or for the detection of chlamydiae in clinical samples.

126 ggests a potential role for gastrointestinal chlamydiae in genital tract pathogenicity.

127 r simultaneous detection of three species of chlamydiae in human and avian specimens.

128 cular genetic analyses regarding the role of chlamydiae in induction of inflammatory arthritis have i

129 ors of peptidoglycan synthesis or culture of chlamydiae in medium lacking tryptophan leads to the for

130 he presence or absence of antibodies against chlamydiae in only 78 and 4.9% of sheep and bovine sera,

131 of the inability of researchers to quantify chlamydiae in semen.

132 delayed the appearance of the peak level of chlamydiae in the animal and decreased the pathological

133 ingly, we detected greater numbers of viable chlamydiae in the oviducts at lower inoculating doses, a

134 nown about the interaction of the phage with chlamydiae in their natural animal host.

135 primary peritoneal neutrophils (PPNs) killed chlamydiae in vitro in an antibody-dependent manner.

136 last several years, four different phages of chlamydiae, in addition to a phage associated with Chlam

137 eterinarians, that in virtually all hosts of chlamydiae, including mammals and birds, chlamydiae resi

138 Our findings reveal a mechanism by which chlamydiae induce localized cytoskeletal changes by the

139 How chlamydiae induce this process is unknown.

140 Cytotoxin gene transcripts were detected in chlamydiae-infected cells, and a protein with the expect

141 which showed no cross-reactivity with other chlamydiae infecting humans.

142 l differentiation of the replicating form of chlamydiae into the infectious form until sufficient rou

143 vitro is defined as viable but noncultivable chlamydiae involving morphologically enlarged, aberrant,

144 The ability to genetically manipulate chlamydiae is a major advancement that will enhance our

145 ta suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infect

146 Cell division in Chlamydiae is poorly understood as apparent homologs to

147 ht on how the construction of a cell wall in chlamydiae is taking shape and why the wall is being bui

148 Although chlamydiae lack many biosynthetic capabilities, they ret

149 t during reductive evolution, the pathogenic chlamydiae lost individual nucleotide transporters, in c

150 properties of Npt1Ct and its conservation in chlamydiae make it a potential target for the developmen

151 ed, a clearer picture of the extent to which Chlamydiae manipulate mammalian cellular processes is be

152 nown about the molecular mechanisms by which Chlamydiae manipulate the mammalian host because they ar

153 s, suggesting that ligation of TLR4 by whole chlamydiae may down-modulate signaling by other TLRs.

154 first evidence that obligately intracellular chlamydiae may encounter acidic conditions.

155 condary chlamydial lung infection eliminated chlamydiae more effectively and generated a lung cytokin

156 hlamydophila genomes shows that, as in other chlamydiae, most of the genome diversity is restricted t

157 Under these conditions, chlamydiae must successfully compete with the host cell

158 However, some groupings (e.g., the chlamydiae, mycoplasmas, and green sulfur bacteria) are

159 multivesicular bodies and the intracellular chlamydiae, neutralization with small interfering RNAs a

160 Chlamydiae obtained eukaryotic host cell cholesterol bot

161 Protegrin-mediated inactivation of chlamydiae occurred rapidly, was relatively independent

162 owed by repeat tests with probes to identify chlamydiae or gonococci.

163 an-intermediate' organisms that includes the Chlamydiae, Orientia tsutsugamushi, Wolbachia and Anapla

164 Furthermore, because GrgA is present only in chlamydiae, our findings highlight how nonconserved regi

165 developmental stages of three environmental chlamydiae: Parachlamydia acanthamoebae, Protochlamydia

166 logy varies dramatically among the different chlamydiae, particularly within the species Chlamydia ps

167 no compelling evidence from gene trees that Chlamydiae played any role in establishing the primary p

168 the C. trachomatis genome has revealed that chlamydiae possess genes that may encode a type III secr

169 Electron micrographs indicate that chlamydiae possess needle filaments, and yet database se

170 Because of the dearth of genetic tools for chlamydiae, previous studies examining secreted proteins

171 Chlamydiae primarily infect epithelial cells, and the in

172 Chlamydiae produce large amounts of heat shock protein 6

173 abbreviated genital infection with virulent chlamydiae promotes anamnestic antibody and T cell respo

174 -d-erythro-sphingos ine as a vital stain for chlamydiae proved to be a sensitive method for identifyi

175 le approaches to the genetic manipulation of chlamydiae raises the possibility of explosive progress

176 On removal of IFN-gamma, chlamydiae rapidly reentered the normal developmental cy

177 ificant increase (P < 0.05) in the amount of chlamydiae recovered from the vaginas of mice that had r

178 Therefore, chlamydiae recruit key regulators of membrane traffickin

179 The chlamydiae remain viable and return to normal growth kin

180 Although chlamydiae remained viable and metabolically active, the

181 underlying the intracellular parasitology of Chlamydiae remains poorly understood.

182 Chlamydiae replicate intracellularly within a vacuole th

183 Chlamydiae replicate intracellularly within a vacuole th

184 Chlamydiae replicate within a nonacidified vacuole, term

185 mance liquid chromatography, suggesting that chlamydiae require a minimum concentration of each amino

186 of chlamydiae, including mammals and birds, chlamydiae reside in the gastrointestinal tract for long

187 For chlamydiae, residence in the synovium in patients with a

188 Given Chlamydiae's extended coevolution with eukaryotic cells,

189 paratus provides support for the notion that chlamydiae secrete proteins via a type III mechanism.

190 results show that DC efficiently phagocytose chlamydiae, secrete IL-12 p40, and present chlamydial an

191 Genomes of all sequenced chlamydiae show the presence of two genes encoding lipoi

192 osis of ruminant infections with abortigenic chlamydiae, since they are more sensitive than the CFT,

193 Chlamydiae sp. are obligate intracellular pathogens that

194 The ability of chlamydiae specifically to bind heparan sulphate or hepa

195 sulfuromonadales, Firmicutes, Bacteroidetes, Chlamydiae, Spirochaeta, and Chloroflexi and two archaea

196 ct immunofluorescence of cells infected with chlamydiae stained with an antibody to the trans-Golgi n

197 c1 on gene expression patterns requires that chlamydiae strictly control Hc1 activity.

198 an and the absence of an FtsZ homolog within chlamydiae suggest an unusual mechanism for the division

199 not further compromise host defense against chlamydiae, suggesting that compensatory mechanisms are

200 he difficulty of growing large quantities of chlamydiae suitable for biochemical fractionation, littl

201 and plants and strengthens the argument that chlamydiae synthesize a cell wall despite the inability

202 These studies revealed two fates for chlamydiae taken onto the lamellipodial surface: 1) some

203 OMs were partially protected, shedding fewer chlamydiae than did control mice.

204 Proteins present in the outer membrane of chlamydiae that are involved in mucosal epithelial cell

205 hyl methanesulfonate mutagenesis to generate chlamydiae that contained less then one mutation per gen

206 Chlamydiae that have been internalized by Fc-mediated en

207 cells are artificially infected with certain chlamydiae that have not been adapted to the host specie

208 Thus, among women with similar exposure to chlamydiae, the serologic response to Hsp10 exhibited a

209 C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures differ considerab

210 are located in a single locus; however, for chlamydiae these genes are scattered throughout the geno

211 uggest that the derivative compounds inhibit chlamydiae through a T3SS-independent mechanism.

212 istence is an alternative life cycle used by chlamydiae to avoid the host immune response.

213 nts of the vaginal microbial flora, allowing chlamydiae to escape IFN-gamma-mediated eradication and

214 o provide a pathogenic mechanism that allows chlamydiae to establish themselves in a site that is not

215 contribute to its ability to bind and bridge chlamydiae to eukaryotic cells.

216 ligand that mediates infectivity by bridging chlamydiae to eukaryotic cells.

217 dary inclusions via IncA-laden fibers allows chlamydiae to generate an expanded intracellular niche i

218 l ancestry, but we detect no strong case for Chlamydiae to host transfer under the best-fitting model

219 provide the basis for the susceptibility of chlamydiae to PG inhibitors.

220 Our findings provide a mechanism for chlamydiae to sense changes in tryptophan levels and to

221 The adhesion of Chlamydiae to the eukaryotic host cell is a pivotal step

222 t least one of these products is secreted by chlamydiae to the inclusion membrane.

223 obviate the need for transport induction by chlamydiae under conditions favoring the growth of infec

224 Chlamydiae undergo a biphasic developmental cycle charac

225 Interestingly, one of the strategies that chlamydiae use for these purposes is the induction of li

226 Unconventionally, Chlamydiae use ROS to their advantage by activating casp

227 From within this protective environment, chlamydiae usurp numerous functions of the host cell to

228 lex developmental cycle, it is possible that chlamydiae utilize a different complement of proteins to

229 When we isolated HrcA from chlamydiae, we only detected the full-length protein, bu

230 Chlamydiae were detected by one or more procedures in 22

231 aces of an ancient link to parasites such as Chlamydiae were found in the genomes of C. paradoxa and

232 Large numbers of chlamydiae were found in vaginal secretions of progester

233 After internalization, these latter chlamydiae were found within intracellular inclusions, w

234 aken onto the lamellipodial surface: 1) some chlamydiae were moved in a random fashion on the cell su

235 Viable gonococci and chlamydiae were recovered for an average of 8 to 10 days

236 ed into the culture medium, whereas 2) other chlamydiae were translocated across the lamellipodium in

237 Chlamydiae, which are obligate intracellular bacteria, r

238 relationship between planctomycetes and the chlamydiae, which has previously been postulated on the

239 Treatment of chlamydiae with inhibitors of peptidoglycan synthesis or

240 Many of the interactions of chlamydiae with the host cell are dependent upon bacteri

241 Moreover, the relationship of chlamydiae with the host cell, in particular its energy

242 tes that they might also be used to identify chlamydiae without culture or isolation.

243 understanding of antimicrobial resistance in chlamydiae would benefit from the development of standar