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1 cterial pathogens Brucella melitensis and B. abortus.
2 ansport has been found to attenuate Brucella abortus.
3 p40 than did mice infected with wild-type B. abortus.
4 teria Agrobacterium tumefaciens and Brucella abortus.
5 evasion of adaptive immune mechanisms by B. abortus.
6 tion rates in animals similar to those of B. abortus.
7 rotein, DNA repair, and SOS regulation in B. abortus.
8 factor for growth and virulence of Brucella abortus.
9 chronic infection of both S. meliloti and B. abortus.
10 or 10(8) inclusion-forming units (IFU) of C. abortus.
11 cattle naturally preexposed to Chlamydophila abortus.
12 am-negative intracellular bacterium Brucella abortus.
13 umefaciens, and the animal pathogen Brucella abortus.
14 val of the global zoonotic pathogen Brucella abortus.
15 ols the cellular and infection biology of B. abortus.
16 induced by injection of heat-killed Brucella abortus.
17 analyzed Erfe-deficient mice injected with B abortus.
18 sis is a unique feature of GSR control in B. abortus.
19 al inoculation of non-pregnant sheep with C. abortus.
20 le explanation for the attenuation of the B. abortus 2,3-DHBA-deficient mutant BHB1 in pregnant rumin
22 tracellular trafficking of virulent Brucella abortus 2308 and attenuated hfq and bacA mutants was fol
23 ned DHBA biosynthesis locus from virulent B. abortus 2308 and genetic complementation of defined Esch
24 roperoxide, but not hydrogen peroxide, in B. abortus 2308 and that OhrR represses the transcription o
25 retic analysis of cell lysates from Brucella abortus 2308 and the isogenic hfq mutant Hfq3 revealed t
26 llular replication, the numbers of acidic B. abortus 2308 BCP decreased while remaining cathepsin D(-
27 ve regulation of mntH expression in Brucella abortus 2308 but also identify the cis-acting elements u
28 nt, designated MEK2, was constructed from B. abortus 2308 by gene replacement, and the sodC mutant ex
29 tectable levels of Irr were found only in B. abortus 2308 cells by Western blot analysis following gr
30 ccine, since protection against wild-type B. abortus 2308 challenge was as effective as that obtained
32 BhuA exhibits maximum expression in Brucella abortus 2308 during growth under iron-deprived condition
33 eins represent important iron sources for B. abortus 2308 during its residence in the mammalian host
34 nated CAM220) derived from virulent Brucella abortus 2308 exhibited increased sensitivity to the alky
35 Ohr plays a prominent role in protecting B. abortus 2308 from organic hydroperoxide stress in in vit
37 ntal findings indicate that SodC protects B. abortus 2308 from the respiratory burst of host macropha
38 es designated BAB2_0837-0840 in the Brucella abortus 2308 genome sequence are predicted to encode a C
39 d as BAB2_0350 and BAB2_0351 in the Brucella abortus 2308 genome sequence are predicted to encode Ohr
40 The gene annotated BAB2_1150 in the Brucella abortus 2308 genome sequence is predicted to encode a ho
41 he gene designated BAB1_1460 in the Brucella abortus 2308 genome sequence is predicted to encode the
42 s, we searched the Brucella suis 1330 and B. abortus 2308 genomes for genes with an upstream virB pro
43 The results of these studies suggest that B. abortus 2308 has at least one other heme oxygenase that
44 ired for the wild-type virulence of Brucella abortus 2308 in mice and indicated that the mntH gene is
45 nscription of the ftrA gene is induced in B. abortus 2308 in response to iron deprivation and exposur
46 on of isogenic mutants derived from Brucella abortus 2308 indicates that the AlcR homolog DhbR (2,3-d
48 oduct, the expression of the mntH gene in B. abortus 2308 is repressed by Mn(2+), but not Fe(2+), and
49 ents a relevant environmental stress that B. abortus 2308 must deal with during its residence in the
51 RNAs, indicating that the AbcR sRNAs from B. abortus 2308 perform redundant regulatory functions.
54 ion of erythritol to low-iron cultures of B. abortus 2308 stimulated the production of 2,3-DHBA by in
55 ponse to iron deprivation in the parental B. abortus 2308 strain, and a direct and specific interacti
56 sponsive two-component regulator in Brucella abortus 2308 that responds to decreasing levels of O(2)
57 tein plays a role in the ability of Brucella abortus 2308 to use heme as an iron source, an isogenic
58 s of an isogenic bhuA mutant derived from B. abortus 2308 verified that there is a link between BhuA
59 he transcriptional start site for mntH in B. abortus 2308 was determined by primer extension analysis
60 somal pathway and replication of virulent B. abortus 2308 within these vesicles corresponds with an i
61 e seen for control particles (heat-killed B. abortus 2308, live Escherichia coli HB101, or latex bead
63 ys an important role in the physiology of B. abortus 2308, particularly during its intracellular surv
66 ction in comparison to its parent strain, B. abortus 2308, when cultured in the presence of erythrito
67 ir and resistance to oxidative killing in B. abortus 2308, XthA-1 is not required for wild-type virul
69 D(+) BCP was significantly lower for live B. abortus 2308-infected cells than for either Brucella mut
74 mentally infected with different doses of C. abortus (5x10(3), 5x10(5) and 5x10(7) inclusion forming
76 ium meliloti, a legume symbiont and Brucella abortus, a phylogenetically related mammalian pathogen,
77 um meliloti, a legume symbiont, and Brucella abortus, a phylogenetically related mammalian pathogen,
81 lence in C57BL/6 and BALB/c mice, but the B. abortus ahpC katE double mutant is extremely attenuated,
82 (astrocytes and microglia) infected with B. abortus also induced activation of HBMEC, but to a great
83 infection, we studied the persistence of B. abortus and an isogenic virB mutant deficient in the Vir
84 rtions supports previous indications that B. abortus and B. melitensis share a common ancestor that d
87 everal fragments were shared between only B. abortus and B. suis, B. abortus shared more fragments an
88 n OPS epitope equally common to all Brucella abortus and Brucella melitensis strains but unique to Br
90 es that are predominantly lytic for Brucella abortus and Brucella neotomae; Group II included Bk, R/C
91 uced by an injection of heat-killed Brucella abortus and examined the contribution of hepcidin by com
92 -type strain of the ovine pathogen Chlamydia abortus and its nitrosoguanidine-induced, temperature-se
94 litensis 16 M would be similar to znuA in B. abortus and questioned whether it may also be an importa
96 To identify in vivo interactions between B. abortus and the host that lead to persistent infection,
103 such as Bacteroides fragilis and Salmonella abortus are observed for CD14(+/+), but not CD14(-/-), m
104 The lipid A molecules of S. meliloti and B. abortus are unusually modified with a very-long-chain fa
108 s also dispensable for the persistence of B. abortus, B. melitensis, and B. suis in mice up to 4 week
109 neotomae is a rodent pathogen, and unlike B. abortus, B. melitensis, and B. suis, B. neotomae has not
112 human and animal origin, including Brucella abortus, B. melitensis, B. ovis, B. neotomae, marine mam
113 ationships of five Brucella species-Brucella abortus, B. melitensis, B. suis, B. canis, and B. ovis-u
116 that form chronic infections, e.g., Brucella abortus, Bartonella henselae, and Legionella pneumophila
117 nt BEA5, and, unlike the parental strain, B. abortus BEA5 cannot utilize heme as an iron source in vi
118 ison of the growth characteristics of the B. abortus bhuA mutant and 2308 in this medium suggested th
120 n 2308, and unlike its parent strain, the B. abortus bhuA mutant is unable to maintain a chronic sple
122 , and Pr phages that are lytic mainly for B. abortus, Brucella melitensis and Brucella suis; Group II
123 of the medically relevant pathogens Brucella abortus, Brucella melitensis, Bartonella henselae, and L
124 ium botulinum, Brucella melitensis, Brucella abortus, Brucella suis, and Brucella canis were extracte
125 , producing four clades as follows: Brucella abortus-Brucella melitensis, Brucella suis-Brucella cani
126 its transcription is strongly induced in B. abortus by various stressors encountered by the bacteria
129 nate immunity of the CNS set in motion by B. abortus contributes to the activation of the blood-brain
132 s uncovered when it was determined that a B. abortus dhbC mutant (BHB1) defective in 2,3-DHBA product
133 tal infection of pregnant cattle with the B. abortus dhbC mutant BHB1 clearly showed that production
134 Introduction of a bhuQ mutation into the B. abortus dhbC mutant BHB2 (which cannot produce sideropho
135 Restoring 2,3-DHBA production to the B. abortus dhbC mutant by genetic complementation abolished
136 ect, suggesting that the inability of the B. abortus dhbC mutant to display wild-type growth in the p
137 analysis showed that transcription of the B. abortus dhbCEBA operon originates from two iron-regulate
138 nking regions immediately adjacent to the B. abortus dhbCEBA operon, suggesting that B. abortus has t
139 al intracellular pathogens, such as Brucella abortus, display a biphasic infection process starting w
142 Signaling pathways triggered by Brucella abortus DNA involves TLR9, AIM2, and stimulator of IFN g
144 the x-ray crystal structures of the Brucella abortus DRL enzyme in its apo form and in complex with t
146 he prokaryotes Brucella melitensis, Brucella abortus, Erythrobacter litoralis, and Pseudomonas syring
147 e use a genomic approach to examine Brucella abortus evolution, cross-species transmission and spatia
148 ort the complete genome sequence of Brucella abortus field isolate 9-941 and compare it to those of B
151 Compared with the parental strain, the B. abortus ftrA mutant displays a decreased capacity to use
154 ia coli mutants were used to identify the B. abortus genes (designated dhbC, -B, and -A) responsible
164 A 640-kb inversion on chromosome II of B. abortus has been reported previously and is further desc
165 . abortus dhbCEBA operon, suggesting that B. abortus has the genetic capacity to produce a more compl
166 sent study the genes regulated by MucR in B. abortus have been elucidated using microarray analysis a
167 _0612 are highly over-produced in a Brucella abortus hfq mutant compared with the parental strain, an
168 factor RpoS in many bacteria, and a Brucella abortus hfq mutant displays a phenotype in vitro, which
170 l DNA in the context of heat-killed Brucella abortus (HKBA) engages TLR9 in dendritic cells (DC), res
173 nd IgG2 serum antibodies against ruminant C. abortus in a chemiluminescent enzyme-linked immunosorben
174 was crucial for increased replication of B. abortus in AAMs, and for chronic infection, as inactivat
178 aintenance of chronic spleen infection by B. abortus in mice, experimental infection of pregnant catt
179 and virB11 are essential for virulence of B. abortus in mice, while functions encoded by the virB1, v
183 iption of cell-cycle progression of Brucella abortus, including unipolar growth and the ordered initi
184 upernatant from macrophages infected with B. abortus induced bone marrow-derived monocytes (BMMs) to
185 Brucella abortus Infection of HBMEC with B. abortus induced the secretion of IL-6, IL-8, and MCP-1,
186 o and in vivo evidence showing that Brucella abortus-induced inflammatory response leads to the activ
187 ate that the cross talk of LX-2 cells and B. abortus induces autophagy and fibrosis with concomitant
188 was dependent on IL-1beta because CS from B. abortus-infected astrocytes and microglia deficient in c
192 bortus, the capacity of supernatants from B. abortus-infected hepatocytes and monocytes to induce MMP
193 icate that activated T cells, elicited by B. abortus-infected macrophages and influenced by the infla
194 eterinarians with occupational exposure to C abortus-infected sheep revealed only sporadic immune res
195 ct antibodies to these surface antigens in C abortus-infected women who had undergone septic abortion
196 e animals were also indirectly exposed to C. abortus infection (cohort challenged) by contact with th
197 sm loads was fivefold more prevalent than C. abortus infection and was most frequently detected by va
199 The present study demonstrates that Brucella abortus infection induces the activation of the autophag
201 BMEC) in response to infection with Brucella abortus Infection of HBMEC with B. abortus induced the s
202 -1 knockout mice were more susceptible to B. abortus infection than were wild-type animals, suggestin
203 the response of macrophages 4 h following B. abortus infection was analyzed to identify early intrace
204 nner et al. (2015) show that during Brucella abortus infection, an endoplasmic reticulum stress senso
209 fic antigen for the serodiagnosis of human C abortus infections was Pmp13G, which showed no cross-rea
211 globulin M and complement-opsonized Brucella abortus infects and survives inside primary murine B cel
218 e obligate intracellular bacterium Chlamydia abortus is the causative agent of enzootic abortion of e
220 itors of intracellular replication reduce B. abortus metabolism in axenic culture and perturb feature
224 o severe human anemia of inflammation, the B abortus model shows multifactorial pathogenesis of infla
227 with B. abortus S2308 or pretreated with B. abortus O polysaccharide did not prevent rough CA180-ind
229 immunosorbent assay with lysed Chlamydophila abortus or Chlamydophila pecorum elementary body antigen
230 hole limpet hemocyanin, heat-killed Brucella abortus, or infection with Nippostrongylus brasiliensis
231 S/SIGNIFICANCE: This study indicates that C. abortus Pmp18D is proteolytically processed at the cell
232 proteins into three distinct clades with C. abortus Pmp18D, being most similar to those originating
233 dings indicate that the 14-kDa protein of B. abortus possesses lectin-like properties and is essentia
236 unctional analyses that demonstrated that B. abortus RadA complements a radA defect in E. coli but co
238 persensitive to UV damage, surprisingly a B. abortus recA null mutant conferred only modest sensitivi
240 y MHC II and allows host control of Brucella abortus replication in IL-4-treated DCs and in RUFY4-exp
241 icacy of these molecules as inhibitors of B. abortus replication in the intracellular niche suggests
242 ytotoxic compounds specifically inhibited B. abortus replication in the intracellular niche, which su
245 -pregnant sheep with a low/medium dose of C. abortus results in a latent infection that leads in a su
247 Furthermore, macrophages preinfected with B. abortus S2308 or pretreated with B. abortus O polysaccha
249 ared between only B. abortus and B. suis, B. abortus shared more fragments and had fewer nucleotide p
252 lling by cultured murine macrophages, the B. abortus sodC mutant also displayed significant attenuati
256 e encoding the 14-kDa protein in virulent B. abortus strain 2308 induced a rough-like phenotype with
257 rotection against challenge with virulent B. abortus strain 2308 or B. suis strain 1330 but no protec
258 tracellular bacterial pathogen Chlamydophila abortus strain S26/3 (formerly the abortion subtype of C
259 en genes, the genetic complements of both B. abortus strains are identical, whereas the three species
261 hyR and sigma(E1), are required for Brucella abortus stress survival in vitro and maintenance of chro
262 how that the intracellular pathogen Brucella abortus survives and replicates preferentially in altern
264 re higher in mice infected with wild-type B. abortus than in mice infected with the virB mutant, as s
267 sette in the intracellular pathogen Brucella abortus that consists of the toxin gene, brnT, and its a
268 teolysis is a novel regulatory feature in B. abortus that ensures proper control of GSR transcription
269 pestis, Francisella tularensis, and Brucella abortus), the last four of which are biothreat agents.
271 Yet, if LX-2 cells are infected with B. abortus, the capacity of supernatants from B. abortus-in
274 or virB11 markedly reduced the ability of B. abortus to persist in the spleens of mice at 8 weeks aft
275 virB locus markedly reduce the ability of B. abortus to survive in cultured macrophages or to persist
276 All mutations reduced the ability of B. abortus to survive in J774A.1 mouse macrophage-like cell
284 ich site is recognized by MucR from Brucella abortus using a similar mechanism involving contacts wit
291 parenchyma upon intracranial injection of B. abortus was diminished in the absence of Nod-like recept
295 key feature of the animal pathogen Chlamydia abortus, where infection remains inapparent in the non-p
296 duction triggered by infection with Brucella abortus, which induces ER stress by injecting the type I
298 S, we compared host responses elicited by B. abortus with those of an isogenic mutant in the virB ope
299 PPARgamma promotes chronic persistence of B. abortus within AAMs, and targeting this pathway may aid
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