ライフサイエンスコーパス: B. bronchiseptica

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

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

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

4 strongly support nosocomial transmission of B. bronchiseptica.

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

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

7 majority of the transcriptional response to B. bronchiseptica.

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

9 including the closely related mouse pathogen B. bronchiseptica.

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

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

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

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

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

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

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

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

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

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

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

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

22 onserved among multiple clinical isolates of B. bronchiseptica.

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

24 large in-frame deletion relative to batB of 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 We previously cloned a B. bronchiseptica (Bb) genomic DNA fragment that complem

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

102 B. bronchiseptica DeltahurI mutant BRM23 was defective i

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

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

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

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

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

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

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

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 B. bronchiseptica expresses fimA in a BvgAS-dependent fa

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

121 B. bronchiseptica fauA insertion mutant BRM17 was unable

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

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

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

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

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

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

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

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

130 Using B. bronchiseptica genetically modified strains deficient

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

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

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

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

135 ched in outer membrane proteins derived from B. bronchiseptica grown at 23 degrees C were not present

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 B. bronchiseptica induced apoptosis in macrophages in vi

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

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

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

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

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

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

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

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

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

167 B. bronchiseptica infection in healthy adults is an unus

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

169 IgA induced by B. bronchiseptica infection predominantly recognized lip

170 understanding the molecular epidemiology of B. bronchiseptica infections.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 expressed only by modulated bvg+ strains of B. bronchiseptica, may play a key role in the initial co

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

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

204 Bordetella pertussis, B. parapertussis, and B. bronchiseptica might be explained by polymorphisms in

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

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

207 A B. bronchiseptica mutant lacking ACT produced more biofi

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

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

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

211 B. bronchiseptica mutants with nonrevertible defects in

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

213 B. bronchiseptica naturally infects a variety of animal

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

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

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

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

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

219 A B. bronchiseptica pagP homologue was identified that is

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

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

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

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

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

225 evel of attachment was seen, suggesting that B. bronchiseptica produces a Bvg-repressed adhesin under

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

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

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

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

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

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

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

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

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

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

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

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

238 A B. bronchiseptica strain deficient in adenylate cyclase-

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

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

241 A B. bronchiseptica strain that was missing dermonecrotic

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

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

244 Other B. bronchiseptica strains from the same phylogenetic lin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

274 We have found that B. parapertussis and B. bronchiseptica, unlike B. pertussis, contain a full-l

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

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

277 This novel B. bronchiseptica vaccine candidate induces strong local

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