ライフサイエンスコーパス: abortus

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

21 A znuA knockout mutation in B. abortus 2308 (DeltaznuA) was constructed and found to be

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

31 Brucella abortus 2308 derivatives with mini-Tn5 insertions in pur

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

36 1 gene product participates in protecting B. abortus 2308 from oxidative damage.

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

47 Maximum expression of bhuA in B. abortus 2308 is observed during stationary phase when th

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

50 rved in the spleens of mice infected with B. abortus 2308 or a virB mutant.

51 RNAs, indicating that the AbcR sRNAs from B. abortus 2308 perform redundant regulatory functions.

52 B. abortus 2308 persisted within these cathepsin D(-), LAMP

53 Mice infected with B. abortus 2308 produced an antibody response to the protei

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

62 In B. abortus 2308, MucR regulates a wide variety of genes who

63 ys an important role in the physiology of B. abortus 2308, particularly during its intracellular surv

64 In contrast to B. abortus 2308, the isogenic hfq and bacA mutants remained

65 Here we present the genome of B. abortus 2308, the virulent prototype biovar 1 strain, an

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

68 Early trafficking events of B. abortus 2308-containing phagosomes (BCP) were indistingu

69 D(+) BCP was significantly lower for live B. abortus 2308-infected cells than for either Brucella mut

70 AbcR1 and AbcR2) have been identified in B. abortus 2308.

71 to wild-type expression of virB in Brucella abortus 2308.

72 ith those of the virulent parental strain B. abortus 2308.

73 isogenic ftrA mutant was constructed from B. abortus 2308.

74 mentally infected with different doses of C. abortus (5x10(3), 5x10(5) and 5x10(7) inclusion forming

75 m the anemia induced by heat-killed Brucella abortus, a model of inflammatory anemia.

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,

78 Two small RNAs in Brucella abortus, AbcR1 and AbcR2, are required for wild-type vir

79 Although B. abortus-activated T cells actively secreted the pro-oste

80 B. abortus ahpC and katE mutants exhibit wild-type virulenc

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

85 d S708 phages that are lytic for B. suis, B. abortus and B. neotomae.

86 In extravillous trophoblasts (EVTs), B. abortus and B. suis replicated within single-membrane ac

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

89 s, manBA, virB2, and asp24, in both Brucella abortus and Brucella melitensis.

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

93 the role of DNA repair networks in Brucella abortus and its role in pathogenesis.

94 litensis 16 M would be similar to znuA in B. abortus and questioned whether it may also be an importa

95 stress survival and the interface between B. abortus and the host immune system.

96 To identify in vivo interactions between B. abortus and the host that lead to persistent infection,

97 he rapid identification of Brucella spp., B. abortus, and B. melitensis in a single test.

98 ed bacteria Sinorhizobium meliloti, Brucella abortus, and Ochrobactrum anthropi.

99 ria mallei, Francisella tularensis, Brucella abortus, and ricin.

100 f 480 known bioactive compounds for novel B. abortus anti-infectives.

101 We demonstrate recognition of B. abortus antibodies through capture by fluorescent silica

102 All anti-C. abortus antibody isotypes increased in heifers following

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

105 other chlamydial species, C. psittaci and C. abortus, are known zoonotic pathogens.

106 Here, we study the cell cycle of B. abortus at the single-cell level, in culture and during

107 Brucella abortus, B. melitensis, and B. suis are pathogenic to hu

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

110 d upon three pathogenic Brucella species: B. abortus, B. melitensis, and B. suis.

111 crodilution susceptibility tests of Brucella abortus, B. melitensis, and B. suis.

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

114 AI was induced with heat-killed Brucella abortus (BA).

115 The B. abortus bab1_1517 mutant strain was significantly attenu

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

119 The B. abortus bhuA mutant HR1703 exhibits significant attenuat

120 n 2308, and unlike its parent strain, the B. abortus bhuA mutant is unable to maintain a chronic sple

121 Although the Brucella abortus bhuQ mutant DCO1 did not exhibit a defect in its

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

127 The results reveal that B. abortus causes a chronic infection of lung tissue in BAL

128 B. abortus cell-cycle progression is coordinated with intra

129 nate immunity of the CNS set in motion by B. abortus contributes to the activation of the blood-brain

130 Within this conserved Cp. abortus core genome we have identified the major regions

131 nce, primers were designed to construct a B. abortus deletion mutant.

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

140 Livers from mice infected with B. abortus displayed a fibrogenic phenotype with patches of

141 Thus, proper control of B. abortus division site polarity is necessary for survival

142 Signaling pathways triggered by Brucella abortus DNA involves TLR9, AIM2, and stimulator of IFN g

143 In dams, C. abortus dominated in milk and C. pecorum dominated in th

144 the x-ray crystal structures of the Brucella abortus DRL enzyme in its apo form and in complex with t

145 The intracellular bacterium Brucella abortus ensures its survival by forming the Brucella-con

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

149 human pathogenic Brucella species and to B. abortus field isolate 9-941.

150 melitensis for sheep and goats, and Brucella abortus for cattle).

151 Compared with the parental strain, the B. abortus ftrA mutant displays a decreased capacity to use

152 The B. abortus ftrA mutant exhibits significant attenuation in

153 The Brucella abortus general stress response (GSR) system is required

154 ia coli mutants were used to identify the B. abortus genes (designated dhbC, -B, and -A) responsible

155 suis or B. melitensis were present in the B. abortus genome.

156 y on day 70 of gestation with 2x10(6) IFU C. abortus (group 5).

157 a protein, which was detected in vitro in B. abortus grown to stationary phase.

158 A genome-scale analysis of the B. abortus GSR regulon identified stress response genes pre

159 of genes that closely overlaps the known B. abortus GSR regulon.

160 LovhK (bab2_0652), functions as a primary B. abortus GSR sensor.

161 The B. abortus GSR signaling pathway has multiple layers of pos

162 Thus, the B. abortus GSR system is dispensable for colonization but i

163 We conclude that the B. abortus GSR system regulates acute stress adaptation and

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

169 ibute to the attenuation displayed by the B. abortus hfq mutant Hfq3 in the mouse model.

170 l DNA in the context of heat-killed Brucella abortus (HKBA) engages TLR9 in dendritic cells (DC), res

171 Heat-killed B. abortus (HKBA) is a strong Th1 adjuvant and carrier.

172 icantly with a rise in postchallenge anti-C. abortus IgM levels over prechallenge levels.

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

175 ired for the wild-type virulence of Brucella abortus in cattle.

176 Thus, opsonized B. abortus in human monocytes survives within phagosomes th

177 tion and further secretion of IL-1beta by B. abortus in macrophages.

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

180 ought to be important to the virulence of B. abortus in pregnant ruminants.

181 nt for the T4SS to mediate persistence of B. abortus in the spleen.

182 Here, we show that a Brucella abortus in-frame mucR deletion strain exhibits a pronoun

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

189 Although B. abortus-infected glial cells secreted IL-1beta and TNF-a

190 nisms of liver immune response induced by B. abortus-infected hepatic stellate cells.

191 In contrast, supernatants from B. abortus-infected hepatocytes and monocytes induce MMP-9

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

198 However, with time, B. abortus infection induced Beclin-1 cleavage with concomi

199 The present study demonstrates that Brucella abortus infection induces the activation of the autophag

200 We demonstrate that Brucella abortus infection inhibits matrix metalloproteinase-9 (M

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

205 tions of Igh6(-/-) mice in the context of B. abortus infection.

206 ssion of proinflammatory cytokines during B. abortus infection.

207 2, and AIM2 KO mice are less resistant to B. abortus infection.

208 he TLR-initiated immune response to Brucella abortus infection.

209 fic antigen for the serodiagnosis of human C abortus infections was Pmp13G, which showed no cross-rea

210 e laboratory diagnosis of human and animal C abortus infections.

211 globulin M and complement-opsonized Brucella abortus infects and survives inside primary murine B cel

212 The models predict that the uterine C. abortus inoculum causing infertility is 8.5-fold higher

213 Chlamydophila abortus is a common cause of ruminant abortion.

214 Brucella abortus is a facultative intracellular pathogen of macro

215 Brucella abortus is a facultative, intracellular zoonotic pathoge

216 Brucella abortus is an intracellular bacterial pathogen and an et

217 Brucella abortus is an intracellular pathogen that persists withi

218 e obligate intracellular bacterium Chlamydia abortus is the causative agent of enzootic abortion of e

219 Significantly, Cp. abortus lacks any toxin genes, and also lacks genes invo

220 itors of intracellular replication reduce B. abortus metabolism in axenic culture and perturb feature

221 Twenty-six compounds inhibited B. abortus metabolism in axenic culture, thirteen of which

222 The B. abortus mntH mutant also exhibits extreme attenuation in

223 The B. abortus mntH mutant MWV15 exhibits increased susceptibil

224 o severe human anemia of inflammation, the B abortus model shows multifactorial pathogenesis of infla

225 A Brucella abortus mutant lacking TcpB fails to reduce levels of MA

226 Furthermore, B. melitensis but not B. abortus nor B. suis interfered with the invasive capacit

227 with B. abortus S2308 or pretreated with B. abortus O polysaccharide did not prevent rough CA180-ind

228 cit systemic infections with either Brucella abortus or B. melitensis at various doses.

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

234 The complete genomic sequence of B. abortus provides an important resource for further inves

235 This proteomic analysis of B. abortus provides novel insights into the mechanisms util

236 unctional analyses that demonstrated that B. abortus RadA complements a radA defect in E. coli but co

237 We considered the possibility that B. abortus RadA might be compensating for the loss of RecA

238 persensitive to UV damage, surprisingly a B. abortus recA null mutant conferred only modest sensitivi

239 E. coli but could not act in place of the B. abortus RecA.

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

243 totoxic to human host cells and attenuate B. abortus replication in the intracellular niche.

244 0, 10(4), 10(5), 10(6), and 10(8) IFU of C. abortus, respectively.

245 -pregnant sheep with a low/medium dose of C. abortus results in a latent infection that leads in a su

246 ugated to type 1 T cell-independent Brucella abortus ring test Ag (BRT).

247 Furthermore, macrophages preinfected with B. abortus S2308 or pretreated with B. abortus O polysaccha

248 rine macrophages were infected with Brucella abortus S2308-derived rough mutant CA180.

249 ared between only B. abortus and B. suis, B. abortus shared more fragments and had fewer nucleotide p

250 hen used to infect macrophages, DeltaznuA B. abortus showed minimal growth.

251 Further study with DeltaznuA B. abortus showed that its virulence in BALB/c mice was att

252 lling by cultured murine macrophages, the B. abortus sodC mutant also displayed significant attenuati

253 The attenuation displayed by the B. abortus sodC mutant in both resting and IFN-gamma-activa

254 The B. abortus sodC mutant was also found to be much more sensi

255 Brucella abortus SodC was monomeric and released by osmotic shock

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

260 nserved signalling pathway that regulates B. abortus stress physiology and infection biology.

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

263 f the PmpD protein in the animal pathogen C. abortus (termed Pmp18D).

264 re higher in mice infected with wild-type B. abortus than in mice infected with the virB mutant, as s

265 response in mice infected with wild-type B. abortus than in mice infected with the virB mutant.

266 n spleens of mice infected with wild-type B. abortus than in virB mutant-infected mice.

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.

270 Brucella abortus, the bacteria responsible for bovine brucellosis

271 Yet, if LX-2 cells are infected with B. abortus, the capacity of supernatants from B. abortus-in

272 In the intracellular pathogen Brucella abortus, the general stress response (GSR) signalling sy

273 on of virB7 did not reduce the ability of B. abortus to persist in spleens of mice.

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

277 In B abortus-treated Hamp-KO compared with WT mice, anemia wa

278 B abortus-treated wild-type mice developed a moderate anem

279 B abortus-treated WT mice developed severe anemia with a h

280 odel was developed with heat-killed Brucella abortus treatment.

281 The Brucella abortus type IV secretion system (T4SS), encoded by the

282 The Brucella abortus type IV secretion system (T4SS), encoded by the

283 The bacterium Brucella abortus uses a type IV secretion system (VirB T4SS) to g

284 ich site is recognized by MucR from Brucella abortus using a similar mechanism involving contacts wit

285 The Brucella abortus virB locus contains 12 open reading frames, term

286 Mice infected with the B. abortus virB mutant elicited smaller increases in serum

287 In the mouse model, a B. abortus virB mutant was initially able to colonize the s

288 The Brucella abortus virB operon, consisting of 11 genes, virB1 to vi

289 The Brucella abortus virB operon, encoding a type IV secretion system

290 e functions as a photoreceptor regulating B. abortus virulence.

291 parenchyma upon intracranial injection of B. abortus was diminished in the absence of Nod-like recept

292 A 14-kDa protein of B. abortus was previously identified to be immunogenic in a

293 Infection of macrophages by B. abortus was stimulated by light in the wild type but was

294 Ovarian pieces from 24 weeks old abortuses were xenografted s.c. to severe combined immun

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

297 spleen during a mixed infection with the B. abortus wild type.

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

300 The B. abortus xthA-1 mutant also displayed reduced resistance

301 Although the B. abortus xthA-1 mutant exhibited increased sensitivity to