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1 h was acquired by lateral gene transfer from Chlamydiae.
2 ensis is a novel organism closely related to chlamydiae.
3 f the missing bricks for the wall, exists in chlamydiae.
4  did not impact development of intracellular chlamydiae.
5 pholipase D (PLD) enzyme family varies among chlamydiae.
6 orate developmental regulation mechanisms in chlamydiae.
7 the site of attachment of surface-associated chlamydiae.
8 nsfer of genes between the rodent-associated Chlamydiae.
9 n of active disease were positive for ocular chlamydiae.
10 e 1 (Th1) response, which effectively clears chlamydiae.
11 nduced artificially with known quantities of chlamydiae.
12 n of the host ERK-cPLA2 signaling pathway by chlamydiae.
13 e of the cycle and in the infectious form of chlamydiae.
14 sglycosylation reactions occur in pathogenic Chlamydiae.
15 er infection, even in the presence of viable chlamydiae.
16 tion required live, transcriptionally active chlamydiae.
17 ndent on the size of the inoculating dose of chlamydiae.
18 centrations sufficient to kill intracellular chlamydiae.
19 d features related to the complex biology of chlamydiae.
20 ing that these genes are conserved among the chlamydiae.
21 osely homologous to those of hsp10s of other chlamydiae.
22 d were also less susceptible to infection by chlamydiae.
23 rescein-1, succinimidyl ester) conjugated to chlamydiae.
24 ectly examined the pH of vesicles containing chlamydiae.
25 t time the presence of PG in a member of the Chlamydiae.
26 ity to survive and are proficient killers of chlamydiae.
27 enes are also found on chromosomes of extant chlamydiae.
28 ce biochemical and physiological analyses of chlamydiae.
29 ired for optimal growth of the intracellular chlamydiae.
30 t AHNAK is transiently recruited by invading chlamydiae.
31 f multivesicular bodies to the intracellular chlamydiae.
32                                              Chlamydiae, a diverse group of obligate intracellular pa
33           Here, we provide evidence that the Chlamydiae, a phylum of strictly host-associated intrace
34          As obligate intracellular bacteria, chlamydiae actively modify their vacuole to exploit host
35              Modifying the ratio of phage to chlamydiae altered the course of infection and affected
36 e and characterized by decreased shedding of chlamydiae and an infection of shorter duration.
37 e shed approximately 3 logs fewer infectious chlamydiae and are protected from genital tract inflamma
38 is and C. pneumoniae MOMP exposure on intact chlamydiae and immunogenic properties might be because t
39 y cluster" was associated to mucosa-adjacent Chlamydiae and Lentisphaerae, and furthermore associated
40  shown to inhibit intracellular infection by chlamydiae and mycobacteria in macrophages.
41 of the GT and may influence the clearance of chlamydiae and the development of tubal pathology.
42 dual deletion mutants were used to transform chlamydiae and the transformants were characterized phen
43  molecular and cellular interactions between chlamydiae and their host and large-scale prospective im
44  Holosporales, Rickettsiales, Legionellales, Chlamydiae, and Babelota, and 258 genomes linked to host
45 ry infection, shed high levels of infectious chlamydiae, and did not resolve the infection until 3 to
46 d spondyloarthritis continue to suggest that chlamydiae, and perhaps other pathogens function in the
47 mbiotic bacteria, including Patescibacteria, Chlamydiae, and predatory Bdellovibrionota, were also pr
48 karyotic cells that were similar to those of chlamydiae, and the microspheres were competitively inhi
49  have included numerous species of bacteria, chlamydiae, and viruses.
50                                              Chlamydiae appeared to exit the cell either (i) through
51  the response was dependent upon the dose of chlamydiae applied.
52         These pathobiotype differences among chlamydiae are also mirrored in their early interactions
53                                              Chlamydiae are bacterial parasites that carry out a dist
54              Overall, our findings show that chlamydiae are capable of the induction of interferon an
55                                              Chlamydiae are defined by a relatively large core genome
56                                              Chlamydiae are highly successful strictly intracellular
57                                              Chlamydiae are important pathogens and symbionts with un
58 s, reminiscent of effects seen in vitro when chlamydiae are incubated with gamma interferon.
59                                              Chlamydiae are intracellular bacteria that develop withi
60 nlike other intracellular bacteria, however, chlamydiae are metabolically inactive extracellularly an
61                                              Chlamydiae are obligate intracellular bacteria that enco
62                                          The chlamydiae are obligate intracellular bacteria that occu
63                                              Chlamydiae are obligate intracellular bacteria that repl
64                                              Chlamydiae are obligate intracellular bacteria that repl
65                                              Chlamydiae are obligate intracellular bacteria that repl
66                                              Chlamydiae are obligate intracellular bacterial pathogen
67                                              Chlamydiae are obligate intracellular bacterial pathogen
68                                              Chlamydiae are obligate intracellular bacterial pathogen
69                                              Chlamydiae are obligate intracellular bacterial pathogen
70                                              Chlamydiae are obligate intracellular gram-negative bact
71                                          The chlamydiae are obligate intracellular parasites that dev
72                                              Chlamydiae are obligate intracellular parasites which mu
73                                              Chlamydiae are obligate intracellular pathogens that can
74                                              Chlamydiae are obligate intracellular pathogens that eff
75                                          The chlamydiae are obligate intracellular pathogens that occ
76                                          The Chlamydiae are obligate intracellular pathogens that rep
77                                  Endocytosed chlamydiae are trafficked to the Golgi region and begin
78                                              Chlamydiae are widespread Gram-negative pathogens of hum
79 dritic cells (DC) pulsed ex vivo with killed chlamydiae as a novel approach to vaccination against ch
80   The enhanced production of this antigen by chlamydiae as a result of iron limitation is of particul
81  type III secretion systems of environmental chlamydiae at macromolecular resolution and find support
82 accompanied by dispersal of the chromatin as chlamydiae become transcriptionally active, although the
83 l cells, indicating that the MOMP and intact chlamydiae bind the same host receptor.
84 assays, IncA was detectable in intracellular chlamydiae but not within the inclusion membrane.
85  followed by conjunctival sampling to detect chlamydiae by commercial polymerase chain reaction.
86 nvestigated in the preferred target cells of chlamydiae, cervical epithelial cells, nor in vaginally
87 , as follows: Actinobacteria, Bacteroidetes, Chlamydiae, Chloroflexi, Euryarchaeota, Firmicutes, Fuso
88                                              Chlamydiae colonize the gastrointestinal tracts of both
89                                              Chlamydiae comprise important pathogenic and symbiotic b
90 rowth and late differentiation, suggest that chlamydiae contained in small non-fusogenic inclusions w
91           The survival of macrophage-adapted chlamydiae correlates with the multiplicity of infection
92 ports an evolutionary relationship among the chlamydiae, cyanobacteria, and plants and strengthens th
93                             Discoveries that chlamydiae deploy an array of anti-host proteins have pl
94 or purify peptidoglycan (PG) from pathogenic Chlamydiae despite genetic and biochemical evidence and
95                  Not all women infected with chlamydiae develop upper genital tract disease, but the
96                                              Chlamydiae dissociate themselves from the endocytic path
97                                     However, chlamydiae do not produce arginine, so they must import
98                                        Thus, chlamydiae do not reside within highly acidic vesicles a
99                  Upon infection with several chlamydiae, each bacterium creates its own inclusion, re
100             Further, we show that strains of chlamydiae encoding the pzPLD, but not a strain lacking
101                             To survive this, chlamydiae enter an alternative developmental state refe
102 ctions have been proposed as a means whereby chlamydiae evade immune resolution of infection.
103  is a safe niche for chlamydial replication, chlamydiae exploit a number of host cell processes, incl
104                                              Chlamydiae express a type III secretion system (T3SS) th
105 oteobacteria, Bacteroidetes, Actinobacteria, Chlamydiae, Firmicutes, and Acidobacteria.
106 e three tests permit ready identification of chlamydiae for diagnostic and epidemiologic study.
107 titively inhibited the infectivity of viable chlamydiae for epithelial cells, indicating that the MOM
108 were also shown to reduce the infectivity of chlamydiae for epithelial cells.
109 l models has been the use of varied doses of chlamydiae for infection in different laboratories.
110                          The pathway used by Chlamydiae for pABA synthesis differs from the canonical
111 uctive chlamydial growth, thereby protecting chlamydiae from bactericidal attack.
112 tion, although very effective in eradicating chlamydiae from genital tissue and preventing upper geni
113  found that Th2-MoPn was unable to eradicate chlamydiae from the genital tract (GT) when it was trans
114 te that the immune system is unable to clear chlamydiae from the gut, so they can remain indefinitely
115 and late T3S inactivation upon detachment of chlamydiae from the inclusion membrane are crucial for c
116 ly NOS2(-/-) mice shed low numbers of viable chlamydiae from the lower genital tract after immunosupp
117 f the treatments affected shedding of viable chlamydiae from the lower urogenital tract, but the admi
118 posed to Desferal: (i) inclusions containing chlamydiae greatly delayed in maturation, (ii) substanti
119                                              Chlamydiae growing in target mucosal human epithelial ce
120 achomatis, to which a protein in extracts of chlamydiae harvested at 23 h after infection binds.
121 he existence of a peptidoglycan cell wall in chlamydiae has been debated for several years.
122          Fortunately, sexual transmission of chlamydiae has been described for the guinea pig model o
123       The existence of peptidoglycan (PG) in chlamydiae has long been debated.
124                    It has been proposed that chlamydiae have a cytotoxic activity that contributes to
125 g dyes, here we show that some environmental chlamydiae have cell wall sacculi consisting of a novel
126         As obligate intracellular pathogens, chlamydiae have evolved sophisticated, yet undefined, me
127 in chlamydia-infected cells, suggesting that chlamydiae have evolved specific mechanisms for modifyin
128 s and recent advances that have revealed how chlamydiae have maintained conserved aspects of T3S whil
129 however efforts to purify PG from pathogenic Chlamydiae have remained unsuccessful.
130     The data presented here demonstrate that chlamydiae have the ability to convert a regulatory mole
131                            We show here that chlamydiae have the ability to interfere with the NF-kap
132                                              Chlamydiae have to replicate within a cytoplasmic vacuol
133                            For this purpose, chlamydiae hijack certain signaling pathways that preven
134 r set of host proteins as did endocytosis of chlamydiae; however, unlike viable chlamydial organisms,
135 atory infiltrate vs effective elimination of chlamydiae in a macrophage-dominated response.
136 he presence or absence of antibodies against chlamydiae in all sheep and bovine sera.
137 rom culture isolates or for the detection of chlamydiae in clinical samples.
138 ggests a potential role for gastrointestinal chlamydiae in genital tract pathogenicity.
139 r simultaneous detection of three species of chlamydiae in human and avian specimens.
140 cular genetic analyses regarding the role of chlamydiae in induction of inflammatory arthritis have i
141 ors of peptidoglycan synthesis or culture of chlamydiae in medium lacking tryptophan leads to the for
142 he presence or absence of antibodies against chlamydiae in only 78 and 4.9% of sheep and bovine sera,
143  of the inability of researchers to quantify chlamydiae in semen.
144 eage-specific niches and a high abundance of chlamydiae in some habitats.
145  delayed the appearance of the peak level of chlamydiae in the animal and decreased the pathological
146 ingly, we detected greater numbers of viable chlamydiae in the oviducts at lower inoculating doses, a
147 nown about the interaction of the phage with chlamydiae in their natural animal host.
148 primary peritoneal neutrophils (PPNs) killed chlamydiae in vitro in an antibody-dependent manner.
149 last several years, four different phages of chlamydiae, in addition to a phage associated with Chlam
150 eterinarians, that in virtually all hosts of chlamydiae, including mammals and birds, chlamydiae resi
151     Our findings reveal a mechanism by which chlamydiae induce localized cytoskeletal changes by the
152                                          How chlamydiae induce this process is unknown.
153  Cytotoxin gene transcripts were detected in chlamydiae-infected cells, and a protein with the expect
154  which showed no cross-reactivity with other chlamydiae infecting humans.
155 l differentiation of the replicating form of chlamydiae into the infectious form until sufficient rou
156 vitro is defined as viable but noncultivable chlamydiae involving morphologically enlarged, aberrant,
157        The ability to genetically manipulate chlamydiae is a major advancement that will enhance our
158 ta suggest that the inflammatory response to chlamydiae is initiated and sustained by actively infect
159                             Cell division in Chlamydiae is poorly understood as apparent homologs to
160 ht on how the construction of a cell wall in chlamydiae is taking shape and why the wall is being bui
161  was monitored by periodic vaginal swabs and chlamydiae isolation.
162                                     Although chlamydiae lack many biosynthetic capabilities, they ret
163 t during reductive evolution, the pathogenic chlamydiae lost individual nucleotide transporters, in c
164 properties of Npt1Ct and its conservation in chlamydiae make it a potential target for the developmen
165 ed, a clearer picture of the extent to which Chlamydiae manipulate mammalian cellular processes is be
166 nown about the molecular mechanisms by which Chlamydiae manipulate the mammalian host because they ar
167 s, suggesting that ligation of TLR4 by whole chlamydiae may down-modulate signaling by other TLRs.
168 first evidence that obligately intracellular chlamydiae may encounter acidic conditions.
169 condary chlamydial lung infection eliminated chlamydiae more effectively and generated a lung cytokin
170 hlamydophila genomes shows that, as in other chlamydiae, most of the genome diversity is restricted t
171                      Under these conditions, chlamydiae must successfully compete with the host cell
172           However, some groupings (e.g., the chlamydiae, mycoplasmas, and green sulfur bacteria) are
173  multivesicular bodies and the intracellular chlamydiae, neutralization with small interfering RNAs a
174                                              Chlamydiae obtained eukaryotic host cell cholesterol bot
175           Protegrin-mediated inactivation of chlamydiae occurred rapidly, was relatively independent
176 owed by repeat tests with probes to identify chlamydiae or gonococci.
177 xtrinsic signals from the host cell or other chlamydiae, or an intrinsic signal such as chlamydial ce
178 an-intermediate' organisms that includes the Chlamydiae, Orientia tsutsugamushi, Wolbachia and Anapla
179 Furthermore, because GrgA is present only in chlamydiae, our findings highlight how nonconserved regi
180  developmental stages of three environmental chlamydiae: Parachlamydia acanthamoebae, Protochlamydia
181 logy varies dramatically among the different chlamydiae, particularly within the species Chlamydia ps
182  no compelling evidence from gene trees that Chlamydiae played any role in establishing the primary p
183  the C. trachomatis genome has revealed that chlamydiae possess genes that may encode a type III secr
184           Electron micrographs indicate that chlamydiae possess needle filaments, and yet database se
185   Because of the dearth of genetic tools for chlamydiae, previous studies examining secreted proteins
186                                              Chlamydiae primarily infect epithelial cells, and the in
187                                              Chlamydiae produce large amounts of heat shock protein 6
188  abbreviated genital infection with virulent chlamydiae promotes anamnestic antibody and T cell respo
189 -d-erythro-sphingos ine as a vital stain for chlamydiae proved to be a sensitive method for identifyi
190 le approaches to the genetic manipulation of chlamydiae raises the possibility of explosive progress
191                     On removal of IFN-gamma, chlamydiae rapidly reentered the normal developmental cy
192 ificant increase (P < 0.05) in the amount of chlamydiae recovered from the vaginas of mice that had r
193                                   Therefore, chlamydiae recruit key regulators of membrane traffickin
194                                          The chlamydiae remain viable and return to normal growth kin
195                                     Although chlamydiae remained viable and metabolically active, the
196 underlying the intracellular parasitology of Chlamydiae remains poorly understood.
197                                              Chlamydiae replicate intracellularly within a vacuole th
198                                              Chlamydiae replicate intracellularly within a vacuole th
199                                              Chlamydiae replicate within a nonacidified vacuole, term
200 mance liquid chromatography, suggesting that chlamydiae require a minimum concentration of each amino
201  of chlamydiae, including mammals and birds, chlamydiae reside in the gastrointestinal tract for long
202                                          For chlamydiae, residence in the synovium in patients with a
203 eased parasitism in horizontally transmitted chlamydiae residing in amoebae was a result of processes
204                                        Given Chlamydiae's extended coevolution with eukaryotic cells,
205 paratus provides support for the notion that chlamydiae secrete proteins via a type III mechanism.
206 results show that DC efficiently phagocytose chlamydiae, secrete IL-12 p40, and present chlamydial an
207                     Genomes of all sequenced chlamydiae show the presence of two genes encoding lipoi
208 osis of ruminant infections with abortigenic chlamydiae, since they are more sensitive than the CFT,
209                                              Chlamydiae sp. are obligate intracellular pathogens that
210                               The ability of chlamydiae specifically to bind heparan sulphate or hepa
211 sulfuromonadales, Firmicutes, Bacteroidetes, Chlamydiae, Spirochaeta, and Chloroflexi and two archaea
212 ct immunofluorescence of cells infected with chlamydiae stained with an antibody to the trans-Golgi n
213 c1 on gene expression patterns requires that chlamydiae strictly control Hc1 activity.
214 an and the absence of an FtsZ homolog within chlamydiae suggest an unusual mechanism for the division
215  not further compromise host defense against chlamydiae, suggesting that compensatory mechanisms are
216 he difficulty of growing large quantities of chlamydiae suitable for biochemical fractionation, littl
217 and plants and strengthens the argument that chlamydiae synthesize a cell wall despite the inability
218         These studies revealed two fates for chlamydiae taken onto the lamellipodial surface: 1) some
219 OMs were partially protected, shedding fewer chlamydiae than did control mice.
220    Proteins present in the outer membrane of chlamydiae that are involved in mucosal epithelial cell
221 hyl methanesulfonate mutagenesis to generate chlamydiae that contained less then one mutation per gen
222                                              Chlamydiae that have been internalized by Fc-mediated en
223 cells are artificially infected with certain chlamydiae that have not been adapted to the host specie
224   Thus, among women with similar exposure to chlamydiae, the serologic response to Hsp10 exhibited a
225 C. burnetii resemble that of Rickettsiae and Chlamydiae, their genome architectures differ considerab
226  are located in a single locus; however, for chlamydiae these genes are scattered throughout the geno
227 uggest that the derivative compounds inhibit chlamydiae through a T3SS-independent mechanism.
228 istence is an alternative life cycle used by chlamydiae to avoid the host immune response.
229 nts of the vaginal microbial flora, allowing chlamydiae to escape IFN-gamma-mediated eradication and
230 o provide a pathogenic mechanism that allows chlamydiae to establish themselves in a site that is not
231 contribute to its ability to bind and bridge chlamydiae to eukaryotic cells.
232 ligand that mediates infectivity by bridging chlamydiae to eukaryotic cells.
233 dary inclusions via IncA-laden fibers allows chlamydiae to generate an expanded intracellular niche i
234 l ancestry, but we detect no strong case for Chlamydiae to host transfer under the best-fitting model
235  provide the basis for the susceptibility of chlamydiae to PG inhibitors.
236         Our findings provide a mechanism for chlamydiae to sense changes in tryptophan levels and to
237                              The adhesion of Chlamydiae to the eukaryotic host cell is a pivotal step
238 t least one of these products is secreted by chlamydiae to the inclusion membrane.
239  obviate the need for transport induction by chlamydiae under conditions favoring the growth of infec
240                                              Chlamydiae undergo a biphasic developmental cycle charac
241    Interestingly, one of the strategies that chlamydiae use for these purposes is the induction of li
242                            Unconventionally, Chlamydiae use ROS to their advantage by activating casp
243     From within this protective environment, chlamydiae usurp numerous functions of the host cell to
244 lex developmental cycle, it is possible that chlamydiae utilize a different complement of proteins to
245                   When we isolated HrcA from chlamydiae, we only detected the full-length protein, bu
246                                              Chlamydiae were detected by one or more procedures in 22
247 aces of an ancient link to parasites such as Chlamydiae were found in the genomes of C. paradoxa and
248                             Large numbers of chlamydiae were found in vaginal secretions of progester
249          After internalization, these latter chlamydiae were found within intracellular inclusions, w
250 aken onto the lamellipodial surface: 1) some chlamydiae were moved in a random fashion on the cell su
251                         Viable gonococci and chlamydiae were recovered for an average of 8 to 10 days
252 ed into the culture medium, whereas 2) other chlamydiae were translocated across the lamellipodium in
253                                              Chlamydiae, which are obligate intracellular bacteria, r
254  relationship between planctomycetes and the chlamydiae, which has previously been postulated on the
255                                 Treatment of chlamydiae with inhibitors of peptidoglycan synthesis or
256                  Many of the interactions of chlamydiae with the host cell are dependent upon bacteri
257                Moreover, the relationship of chlamydiae with the host cell, in particular its energy
258 tes that they might also be used to identify chlamydiae without culture or isolation.
259 understanding of antimicrobial resistance in chlamydiae would benefit from the development of standar

 
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