ライフサイエンスコーパス: B. bronchiseptica

1 onserved among multiple clinical isolates of B. bronchiseptica.

2 hich CyaA is not critical for the success of B. bronchiseptica.

3 large in-frame deletion relative to batB of B. bronchiseptica.

4 he development of cell-free vaccines against B. bronchiseptica.

5 y tracts of mice more rapidly than wild-type B. bronchiseptica.

6 amined nasal tissues from mice infected with B. bronchiseptica.

7 strongly support nosocomial transmission of B. bronchiseptica.

8 effectively reduced ciliary binding by Bvg+ B. bronchiseptica.

9 compared with BMDCs treated with heat-killed B. bronchiseptica.

10 majority of the transcriptional response to B. bronchiseptica.

11 ximal biofilm formation in the Bvgi phase in B. bronchiseptica.

12 including the closely related mouse pathogen B. bronchiseptica.

13 adhesion to an adhesion deficient strain of B. bronchiseptica.

14 ay an important role in the pathogenicity of B. bronchiseptica.

15 osynthesis was prevented in B. pertussis and B. bronchiseptica.

16 biosynthesis of Bps and biofilm formation by B. bronchiseptica.

17 genes, did not silence expression of bfrD in B. bronchiseptica.

18 eptica or B. pertussis inhibited shedding of B. bronchiseptica.

19 ammation in the lungs of mice than wild-type B. bronchiseptica.

20 felis, 5 for FCV, 1 for C. felis, and 0 for B. bronchiseptica.

21 includes B. pertussis, B. parapertussis, and B. bronchiseptica.

22 hown to be required for optimal virulence of B. bronchiseptica.

23 ependent gene regulation would also occur in B. bronchiseptica.

24 d fur1, one of two fur homologues carried by B. bronchiseptica.

25 isolates of Bordetella spp., including 4 of B. bronchiseptica, 5 of B. parapertussis, and 5 of B. pe

26 In B. bronchiseptica, a remarkable spectrum of expression s

27 In this study, we examined the effects of B. bronchiseptica ACT and TTSS on murine bone marrow-der

28 Wild-type B. bronchiseptica activated the ERK 1/2 signaling pathwa

29 Previous studies indicate that B. bronchiseptica adenylate cyclase toxin (ACT) and the

30 ed simultaneously to probes derived from the B. bronchiseptica alcA gene and the P. multocida toxA ge

31 B. bronchiseptica also infects humans, thereby demonstra

32 compared wbm deletion (Deltawbm) mutants of B. bronchiseptica and B. parapertussis in a variety of a

33 Mutations in the locus in B. bronchiseptica and B. parapertussis prevent O-antigen

34 The B. bronchiseptica and B. parapertussis recipients were n

35 e identification of a large genetic locus in B. bronchiseptica and B. parapertussis that is required

36 parapertussis(hu)) and non-human-infective (B. bronchiseptica and B. parapertussis(ov)) strains.

37 In B. bronchiseptica and B. parapertussis, delta wlb mutant

38 zation contributes to the in vivo fitness of B. bronchiseptica and B. pertussis.

39 icited cross-species protection against both B. bronchiseptica and Bordetella pertussis.

40 le to infection with relatively low doses of B. bronchiseptica and in vivo neutralization studies ind

41 lities to promote the growth of iron-starved B. bronchiseptica and induce bfeA transcription.

42 the terminal trisaccharide, while wild-type B. bronchiseptica and mutants lacking only the palmitoyl

43 that information obtained studying FHA using B. bronchiseptica and natural-host animal models should

44 igated the role of PRN in pathogenesis using B. bronchiseptica and natural-host animal models.

45 tanding the successful zoonotic potential of B. bronchiseptica and other zoonotic bacteria.

46 as amplifying and disseminating vectors for B. bronchiseptica and reveal an important role for the B

47 PS mutants generated in B. parapertussis and B. bronchiseptica and the first deep rough mutants of an

48 re part of a type III secretion apparatus in B. bronchiseptica and three secreted proteins.

49 ny lift-hybridization assay for detection of B. bronchiseptica and toxigenic P. multocida that can be

50 ntly decreased compared to that of wild-type B. bronchiseptica and was below the limit of detection a

51 cells and T cells were highly susceptible to B. bronchiseptica and were killed by intranasal inoculat

52 piratory diseases in a long list of animals (B. bronchiseptica) and whooping cough in humans (B. pert

53 rative analysis of the Bordetella pertussis, B. bronchiseptica, and B. parapertussis genome assemblie

54 Most studies addressing virulence factors of B. bronchiseptica are based on isolates derived from hos

55 Bordetella pertussis, B. parapertussis, and B. bronchiseptica are closely related species associated

56 s report, the fhaB genes of B. pertussis and B. bronchiseptica are functionally interchangeable, at l

57 ent with the idea that the O-antigen loci of B. bronchiseptica are horizontally transferred between s

58 B. pertussis and B. bronchiseptica are most appropriately classified as s

59 enaline augmented transferrin utilization by B. bronchiseptica, as well as siderophore function in vi

60 RB63 than in animals infected with wild-type B. bronchiseptica at 10 days postinoculation.

61 specimens were identified as B. holmesii or B. bronchiseptica at CDC.

62 dence when produced from multicopy plasmids, B. bronchiseptica B013N alcR partially suppressed the al

63 id-borne alcR genes of B. pertussis UT25 and B. bronchiseptica B013N to complement the alcR defect of

64 Additionally, B. pertussis and B. bronchiseptica bfeR mutants exhibited impaired growth

65 rast, bfeA transcription in B. pertussis and B. bronchiseptica bfeR mutants was completely unresponsi

66 ene fusion analyses found that expression of B. bronchiseptica bfrA was increased during iron starvat

67 functional in B. bronchiseptica, but neither B. bronchiseptica bfrD nor bfrE imparted catecholamine u

68 In parallel studies, B. bronchiseptica bhu sequences were also identified and

69 ica bhu sequences were also identified and a B. bronchiseptica bhuR mutant was constructed and confir

70 These results suggest that B. bronchiseptica biofilm formation is growth phase depe

71 Analyses of the extracellular components of B. bronchiseptica biofilm matrix revealed that the major

72 or the formation and complex architecture of B. bronchiseptica biofilms.

73 a protein in immunoblots of B. pertussis and B. bronchiseptica but not B. parapertussis.

74 Neutropenic mice were similarly killed by B. bronchiseptica but not B. pertussis infection, sugges

75 orrespondingly, TLR4 is critical in limiting B. bronchiseptica but not B. pertussis or B. parapertuss

76 ively transferred antibodies rapidly cleared B. bronchiseptica but not human pathogens.

77 lonization of the mouse respiratory tract by B. bronchiseptica, but is required for persistence of th

78 B. pertussis were shown to be functional in B. bronchiseptica, but neither B. bronchiseptica bfrD no

79 Further studies using a B. bronchiseptica bvgAS mutant expressing the B. pertuss

80 ssociated with virulence in B. pertussis and B. bronchiseptica (bvgS, fhaB, fhaC, and fimC) were iden

81 tussis are predominantly differentiated from B. bronchiseptica by large, species-specific regions of

82 ith anti-BcfA serum enhances phagocytosis of B. bronchiseptica by murine macrophages.

83 at growth phase-dependent gene regulation in B. bronchiseptica can function independently from the Bv

84 We further demonstrate that B. bronchiseptica can modulate normal macrophage functio

85 hormones also induce bfeA transcription and B. bronchiseptica can use the catecholamine noradrenalin

86 pertussis can also cause whooping cough, and B. bronchiseptica causes chronic respiratory infections

87 ictly adapted to the human body temperature, B. bronchiseptica causes infection in a broad range of a

88 While B. bronchiseptica causes lethal disease in TLR4-deficien

89 f virulence factors at 24 degrees C, whereas B. bronchiseptica cells resumed the production only upon

90 compared bipA alleles across members of the B. bronchiseptica cluster, which includes both human-inf

91 lution of host adaptation in lineages of the B. bronchiseptica cluster.

92 B. bronchiseptica colonization in IL-10(-/-) mice was si

93 ction model, mutation of arnT did not affect B. bronchiseptica colonization, growth, persistence thro

94 the cyaA promoter or in the bvgAS alleles of B. bronchiseptica compared to B. pertussis, but appears

95 ly increased in mice infected with wild-type B. bronchiseptica compared with mice infected with TTSS

96 lity loci indicated an increased capacity in B. bronchiseptica, compared to B. pertussis, for ex vivo

97 Remarkably, B. bronchiseptica continues to be transferred with the a

98 B. pertussis and B. bronchiseptica core OS were bound to aminooxylated BS

99 scriptome and CGH analysis, we report that a B. bronchiseptica cystic fibrosis isolate, T44625, conta

100 A mutant of B. bronchiseptica defective for hurP was incapable of re

101 B. bronchiseptica DeltahurI mutant BRM23 was defective i

102 In this study, B. pertussis and B. bronchiseptica DeltahurI mutants, predicted to lack a

103 Data presented here confirm that a B. bronchiseptica deltapagP mutant demonstrates defectiv

104 esized that the defective persistence of the B. bronchiseptica deltapagP mutant was due to an increas

105 of the tracheas and lungs of mice, while the B. bronchiseptica Deltawbm mutant showed almost no defec

106 Interestingly, the B. bronchiseptica Deltawlb strain was defective, compare

107 ned that the expression of this homologue in B. bronchiseptica (designated bscN) is regulated by bvg.

108 tudy, we identified an open reading frame in B. bronchiseptica, designated bcfA (encoding BcfA [borde

109 The deletion of btrS in B. bronchiseptica did not affect colonization or initial

110 onary phases, we found that the adherence of B. bronchiseptica did not decrease in these later phases

111 and invasins, deletion of this protein from B. bronchiseptica did not result in any significant defe

112 A fourth protein, Bb2785 from B. bronchiseptica, did not have d-aminoacylase activity.

113 repressed during infection, confirming that B. bronchiseptica does not modulate to the Bvg(-) phase

114 These data suggest that B. bronchiseptica drive DC into a semimature phenotype b

115 rved that <100 colony-forming units (CFU) of B. bronchiseptica efficiently infected mice and displace

116 acteria that serve as an amoeba food source, B. bronchiseptica evades amoeba predation, survives with

117 (BMDCs) from C57BL/6 mice infected with live B. bronchiseptica exhibited high surface expression of M

118 o complement killing assay demonstrated that B. bronchiseptica exhibits pagP-dependent resistance to

119 , these findings suggest that virulent-state B. bronchiseptica expresses multiple adhesins with overl

120 B. bronchiseptica fauA insertion mutant BRM17 was unable

121 FHA(Bp) was able to substitute for FHA from B. bronchiseptica (FHA(Bb)) with regard to its ability t

122 imN protein has 59.4 and 52.2% homology with B. bronchiseptica Fim2 and Fim3, respectively, and is si

123 Our results show that B. bronchiseptica flagellin is a potent proinflammatory

124 Our results show that B. bronchiseptica flagellin is able to signal effectivel

125 epithelial cells, we studied the effects of B. bronchiseptica flagellin on host defense responses.

126 ated receptor specificity in the response to B. bronchiseptica flagellin.

127 -producing cells and delays the clearance of B. bronchiseptica from the lungs.

128 esponse led to phagocytosis and clearance of B. bronchiseptica from the lungs.

129 Using B. bronchiseptica genetically modified strains deficient

130 The B. bronchiseptica genome encodes a total of 19 known and

131 In silico searches of the B. bronchiseptica genome to identify other genes that en

132 ene was isolated from a cosmid prepared with B. bronchiseptica genomic DNA that restored normal prope

133 Like E. coli GmhB, B. bronchiseptica GmhB and M. loti GmhB prefer the beta-

134 the sole NAD precursor, quinolinate promoted B. bronchiseptica growth, and the ability to use it requ

135 While B. bronchiseptica has a wide host range, B. pertussis an

136 infection, Bvg-regulated gene activation in B. bronchiseptica has not been investigated in vivo.

137 cell system allows for assessment of initial B. bronchiseptica-host cell interactions that can contri

138 We hypothesize that hemin is acquired by B. bronchiseptica in a BhuR-dependent manner after spont

139 globin was not required to support growth of B. bronchiseptica in an Fe-limiting environment.

140 eltaprn mutant did not differ from wild-type B. bronchiseptica in its ability to adhere to epithelial

141 ophils (PMN) are critical for the control of B. bronchiseptica in mice, our data support the hypothes

142 ay RP, the Aries BA did not cross-react with B. bronchiseptica in our study, although a larger sample

143 sis (FHA(Bp)) and compared it with wild-type B. bronchiseptica in several natural-host infection mode

144 of the bpsABCD locus to the pathogenesis of B. bronchiseptica in swine, the KM22Deltabps mutant was

145 tribution of the T3SS to the pathogenesis of B. bronchiseptica in swine, we compared the abilities of

146 se-dependent contribution to pathogenesis of B. bronchiseptica in swine, we constructed a series of i

147 y infection and host-to-host transmission of B. bronchiseptica in swine.

148 o ciliary binding, we used mutant strains of B. bronchiseptica in the binding assay.

149 es that allow the persistent colonization of B. bronchiseptica in the host respiratory tract.

150 ation of the pagP gene on the persistence of B. bronchiseptica in the lower respiratory tract of mice

151 e, likely contributing to the persistence of B. bronchiseptica in the respiratory tract.

152 passive immunization led to the reduction of B. bronchiseptica in the tracheas and lungs.

153 ce were defective in reducing the numbers of B. bronchiseptica in the upper respiratory tract compare

154 arison of a Delta bipA strain with wild-type B. bronchiseptica indicated that BipA is not required fo

155 ltafhaS strain was out-competed by wild-type B. bronchiseptica, indicating that fhaS is expressed in

156 B. bronchiseptica induced apoptosis in macrophages in vi

157 A strain isolated from a host with B. bronchiseptica-induced disease, strain 1289, was 60-f

158 Interestingly, B. bronchiseptica induces a TLR4-dependent cytokine resp

159 ble and provided evidence that FHA-deficient B. bronchiseptica induces more inflammation in the lungs

160 However, B. bronchiseptica-infected BMDCs did not exhibit signifi

161 In this study, we show that B. bronchiseptica-infected macrophages can induce IL-17

162 CD4+ splenocytes, and that lung tissues from B. bronchiseptica-infected mice exhibit a strong Th17 im

163 nificant role played by neutrophils early in B. bronchiseptica infection and by acquired immunity at

164 tem contributes to pulmonary host defense in B. bronchiseptica infection by recruiting lymphocytes an

165 Y) of host cells are dephosphorylated during B. bronchiseptica infection in a TTSS-dependent manner.

166 B. bronchiseptica infection in healthy adults is an unus

167 n IgA response contributes to the control of B. bronchiseptica infection of the upper respiratory tra

168 IgA induced by B. bronchiseptica infection predominantly recognized lip

169 understanding the molecular epidemiology of B. bronchiseptica infections.

170 The TTSS of B. bronchiseptica inhibits the generation of IFN-gamma-p

171 s suggest that type III-secreted products of B. bronchiseptica interact with components of both innat

172 demonstrate that norepinephrine facilitates B. bronchiseptica iron acquisition from the iron carrier

173 Additionally, B. bronchiseptica is capable of establishing long-term o

174 obust inflammatory response to FHA-deficient B. bronchiseptica is characterized by the early and sust

175 The Bvg- phase of B. bronchiseptica is characterized by the expression of

176 As a species, B. bronchiseptica is more resistant to complement than B

177 Therefore, production of DNT by B. bronchiseptica is necessary to produce the lesions of

178 these results that siderophore production by B. bronchiseptica is not essential for colonization of s

179 es, including those required for motility in B. bronchiseptica, is activated and genes encoding virul

180 (whooping cough), whereas their progenitor, B. bronchiseptica, is of variable virulence in a wide va

181 An extensive characterization of human B. bronchiseptica isolates is needed to better understan

182 The fimbrial phenotype of B. bronchiseptica isolates is usually defined serologica

183 to 10-kb range, which readily discriminated B. bronchiseptica isolates, resulting in 48 fingerprint

184 Cross-reactivity was found only with 5 B. bronchiseptica isolates, which were positive with IS1

185 genes, BteA is secreted through the TTSS of B. bronchiseptica, it is required for cytotoxicity towar

186 An in-frame deletion of bscN in B. bronchiseptica leads to decreased secretion of severa

187 la antibodies protected SCID-beige mice from B. bronchiseptica lethal infection.

188 B. pertussis are independent derivatives of B. bronchiseptica-like ancestors.

189 d B. parapertussis evolved separately from a B. bronchiseptica-like progenitor to naturally infect on

190 the model that BhuR is a hemin receptor and B. bronchiseptica likely acquires heme during infection

191 is involved in the increased virulence of a B. bronchiseptica lineage which appears to be disproport

192 These data are consistent with the view that B. bronchiseptica lineages can have different levels of

193 quired for addition of glucosamine (GlcN) to B. bronchiseptica lipid A.

194 eir endotoxins using RAW cells suggests that B. bronchiseptica lipopolysaccharide (LPS) is 10- and 10

195 f a palmitoyl group to the lipid A region of B. bronchiseptica lipopolysaccharide.

196 The DNA sequence of the B. bronchiseptica locus has been determined and the pres

197 t respond to TNFalpha activation, suggesting B. bronchiseptica may modulate host immunity by inactiva

198 ngs indicate that persistent colonization by B. bronchiseptica may rely on the ability of the bacteri

199 perature adaptation between B. pertussis and B. bronchiseptica may result from selective adaptation o

200 This investigation characterizes a new B. bronchiseptica mechanism for iron uptake from transfe

201 results indicate a critical role for FHA in B. bronchiseptica-mediated immunomodulation, and they su

202 ting that wlb-dependent LPS modifications in B. bronchiseptica modulate interactions with adaptive im

203 For successful colonization, B. bronchiseptica must acquire iron (Fe) from the infect

204 A B. bronchiseptica mutant lacking ACT produced more biofi

205 -A was found to aggregate and permeabilize a B. bronchiseptica mutant lacking the terminal trisacchar

206 ith the observation that a Bvg+ phase-locked B. bronchiseptica mutant was indistinguishable from the

207 efficiently acquired by B. parapertussis and B. bronchiseptica mutants lacking O antigen.

208 B. bronchiseptica mutants with nonrevertible defects in

209 d-type LPS phenotype in the B. pertussis and B. bronchiseptica mutants.

210 B. bronchiseptica naturally infects a variety of animal

211 This study specifically shows that B. bronchiseptica not only inhabits amoebas but can pers

212 Vaccination with heat-killed whole-cell B. bronchiseptica or B. pertussis inhibited shedding of

213 trisaccharide plus an O-antigen-like repeat (B. bronchiseptica), or an altered trisaccharide plus an

214 he heterologous wlb locus from B. pertussis, B. bronchiseptica, or Bordetella parapertussis eliminate

215 These data suggest that B. bronchiseptica pagP encodes a Bvg-regulated lipid A p

216 A B. bronchiseptica pagP homologue was identified that is

217 analysis demonstrated that the lipid A of a B. bronchiseptica pagP mutant differed from wild-type li

218 The wild-type B. bronchiseptica parent strain grown under low-iron con

219 y tract (LRT) sensor], which is required for B. bronchiseptica persistence in the LRT.

220 A revised system for classifying B. bronchiseptica pertactin variants is proposed.

221 The O antigen and palmitoylated lipid A of B. bronchiseptica play no role in this resistance.

222 We sequenced the genomes of B. bronchiseptica RB50 (5,338,400 bp; 5,007 predicted ge

223 Wild-type B. bronchiseptica (RB50) preferentially adhered to cilia

224 rototype strains of B. pertussis (Tohama I), B. bronchiseptica (RB50), and other isolates of B. parap

225 onsiderably lesser extent when compared with B. bronchiseptica Remarkably, B. pertussis maintained th

226 n and myoglobin as sources of nutrient Fe by B. bronchiseptica requires expression of BhuR, an outer

227 n using cloned alcS genes of B. pertussis or B. bronchiseptica restored the wild-type phenotype to th

228 Norepinephrine treatment of B. bronchiseptica resulted in BfeR-dependent bfeA transc

229 ers of wild type, but not type III deficient B. bronchiseptica resulted in rapid aggregation of NF-ka

230 th phase-dependent gene regulation occurs in B. bronchiseptica, resulting in prominent temporal shift

231 alysis of Bvg regulation in B. pertussis and B. bronchiseptica revealed a relatively conserved Bvg(+)

232 t, immunization strategies aimed at inducing B. bronchiseptica-specific IgA may be beneficial to prev

233 ptica B013N to complement the alcR defect of B. bronchiseptica strain BRM13 (Delta alcR1 alcA::mini-T

234 A B. bronchiseptica strain deficient in adenylate cyclase-

235 ute versus chronic disease, we constructed a B. bronchiseptica strain expressing FHA from B. pertussi

236 ronchicine and provided protection against a B. bronchiseptica strain isolated from a dog with kennel

237 (LCVs) from the lungs of mice infected with B. bronchiseptica strain RBX9, which contains an in-fram

238 A B. bronchiseptica strain that was missing dermonecrotic

239 We have constructed a Fim(-) B. bronchiseptica strain, RB63, by introducing an in-fra

240 protected against challenge with a prototype B. bronchiseptica strain.

241 fingerprint profile of chromosomal DNA from B. bronchiseptica strains digested with HinfI or AluI.

242 Other B. bronchiseptica strains from the same phylogenetic lin

243 Four B. bronchiseptica strains possessed the brkA gene; howev

244 Multilocus sequence typing analysis of 49 B. bronchiseptica strains was used to build a phylogenet

245 All bipA genes present in B. bronchiseptica strains were identical to bipA of RB50

246 When 18 additional B. bronchiseptica strains were serotyped, all were found

247 of infection, we found that the virulence of B. bronchiseptica strains, as measured by the mean letha

248 that are protective against highly divergent B. bronchiseptica strains, preventing colonization in th

249 When compared to Bvg+ or Bvg- phase-locked B. bronchiseptica strains, single-knockout strains lacki

250 compared with the levels in B. pertussis and B. bronchiseptica strains.

251 se loci are horizontally transferred between B. bronchiseptica strains.

252 IFN-gamma production by the TTSS facilitates B. bronchiseptica survival in the lower respiratory trac

253 d a series of isogenic mutants in a virulent B. bronchiseptica swine isolate and compared each mutant

254 FHA or the PRN structural gene in a virulent B. bronchiseptica swine isolate.

255 gene, is activated substantially earlier in B. bronchiseptica than B. pertussis following a switch f

256 B. parapertussis are more closely related to B. bronchiseptica than they are to each other, they shar

257 B. parapertussis was more similar to B. bronchiseptica than to B. pertussis in many assays, i

258 The prolonged persistence of B. bronchiseptica that was observed in gamma interferon

259 rs of the genus Bordetella (B. pertussis and B. bronchiseptica) that infect mammals, B. avium binds p

260 Unlike wild-type B. bronchiseptica, the Deltaprn mutant was unable to cau

261 When applied to B. bronchiseptica, the screen identified the first TTSS

262 rY-family sensor kinases and is required for B. bronchiseptica to colonize and persist in the lower,

263 cifically, FHA(Bb), but not FHA(Bp), allowed B. bronchiseptica to colonize the lower respiratory trac

264 ver, FhaS was unable to mediate adherence of B. bronchiseptica to epithelial cell lines in vitro and

265 iae are involved in enhancing the ability of B. bronchiseptica to establish tracheal colonization and

266 onstrating a stable relationship that allows B. bronchiseptica to expand and disperse geographically

267 nes of Paraburkholderia phytofirmans allowed B. bronchiseptica to grow in the absence of supplied pyr

268 se results suggest that pagP is required for B. bronchiseptica to resist antibody-mediated complement

269 ally its catalytic activity, is required for B. bronchiseptica to resist phagocytic clearance but is

270 vivo mouse studies, we hypothesized that the B. bronchiseptica type III secretion system (T3SS) would

271 The B. bronchiseptica type III secretion system (TTSS) media

272 These findings suggest that B. bronchiseptica use the TTSS to rapidly drive respirat

273 Most studies addressing virulence factors of B. bronchiseptica utilize isolates derived from hosts ot

274 This novel B. bronchiseptica vaccine candidate induces strong local

275 Furthermore, human B. bronchiseptica vaccines are not available.

276 ization factor A (BcfA) to develop acellular B. bronchiseptica vaccines in the absence of an addition

277 Despite the widespread use of veterinary B. bronchiseptica vaccines, there is limited information

278 viously for B. pertussis, bfrD expression in B. bronchiseptica was also dependent on the BvgAS virule

279 ed to demonstrate that the rate of growth of B. bronchiseptica was directly correlated with the rate

280 B. bronchiseptica was dramatically more active than B. p

281 ild-type and LPS mutants of B. pertussis and B. bronchiseptica was examined.

282 Expression of nadC in B. bronchiseptica was influenced by nicotinic acid and b

283 B. bronchiseptica was investigated because it is easier

284 thermore, production of BhuR by iron-starved B. bronchiseptica was markedly enhanced by culture in he

285 While wild-type B. bronchiseptica was shed from colonized mice and effic

286 In this study, B. bronchiseptica was shown to use catecholamines to obt

287 B. bronchiseptica was, however, killed by immune serum i

288 formed by the sequenced laboratory strain of B. bronchiseptica We hypothesized that swine isolates wo

289 cell death, type III-secreted proteins from B. bronchiseptica were analyzed using matrix-assisted la

290 Wild-type B. pertussis and B. bronchiseptica were both resistant to SP-D; however,

291 me alcR deletion mutants of B. pertussis and B. bronchiseptica were constructed, and the defined muta

292 tional regulators that were Bvg regulated in B. bronchiseptica were deleted, inactivated, or unregula

293 show that the cyaA genes of B. pertussis and B. bronchiseptica, which encode adenylate cyclase toxin

294 owed that the fhaB genes of B. pertussis and B. bronchiseptica, which encode filamentous hemagglutini

295 of a genetically engineered double mutant of B. bronchiseptica, which lacks adenylate cyclase and typ

296 Using B. bronchiseptica, which naturally infects mice, we show

297 B. bronchiseptica, which was highly resistant to naive s

298 tor 4 (TLR4) in immunity to B. pertussis and B. bronchiseptica, while no role for TLR4 during B. para

299 epithelial cell interactions, we coincubated B. bronchiseptica with rabbit tracheal explant cultures

300 Furthermore, B. bronchiseptica within the sori can efficiently infect