ライフサイエンスコーパス: B. burgdorferi

1 B. burgdorferi 6S RNA (Bb6S RNA) binds to RNA polymerase

2 B. burgdorferi antigen was detected in the DRG and dorsa

3 B. burgdorferi appears to lack the metabolic capacity fo

4 B. burgdorferi cannot utilize the other product of LuxS,

5 B. burgdorferi elongates from discrete zones that are bo

6 B. burgdorferi enters the skin, disseminates via the blo

7 B. burgdorferi has an FlhF homolog (BB0270).

8 B. burgdorferi linear plasmid 36 (lp36) is critical for

9 B. burgdorferi sensu stricto and B. garinii established

10 B. burgdorferi was detected using T2MR in 2/2 (100%) of

11 B. burgdorferi was weakly amplified from one pool using

12 B. burgdorferi-infected mice were subjected to secondary

13 Furthermore, characterization of the 6042 B. burgdorferi TSSs reveals a variety of RNAs including

14 ere selected from our initial analysis of 62 B. burgdorferi surface proteins and synthetic peptides b

15 opose that CheY2 serves as a regulator for a B. burgdorferi virulence determinant that is required fo

16 his end, a bb0744 deletion was isolated in a B. burgdorferi strain B31 infectious background, complem

17 e in vivo findings were corroborated using a B. burgdorferi N40-infected I. scapularis infestation mo

18 Reliable direct-detection methods for active B. burgdorferi infection have been lacking in the past b

19 In addition, B. burgdorferi encodes a second Lon homolog called Lon-1

20 Furthermore, non-adherent B. burgdorferi strain expressing TP0435 acquires the abi

21 ctively primed and T(FH) cells induced after B. burgdorferi infection.

22 existing at the time of, and possibly after, B. burgdorferi infection may play an important role in l

23 nd humans with detectable antibodies against B. burgdorferi are significantly more often MBL deficien

24 ompared to humans without antibodies against B. burgdorferi.

25 , azlocillin has shown good efficacy against B. burgdorferi in mice model.

26 al inhibitory concentration, < 1 nM) against B. burgdorferi, Borrelia afzelii, and Borrelia garinii,

27 e role of MBL in the immune response against B. burgdorferi in more detail.

28 al role in the early immune response against B. burgdorferi We investigated the response of DCs to tw

29 However, although B. burgdorferi contains cholesterol lipids, it lacks sph

30 of nymphal ticks suggest that B. mayonii and B. burgdorferi may have different metabolic capabilities

31 (DeltaVlsE) at day 28 p.i., the active anti-B. burgdorferi immune response did not prevent DeltaVlsE

32 ri spirochete is effectively cleared by anti-B. burgdorferi antibodies of New Zealand White rabbits,

33 ese findings they also developed higher anti-B. burgdorferi IgG serum antibodies compared to WT contr

34 Mouse anti-B. burgdorferi serum was cross-reactive to all recombina

35 test if any significant changes in the anti-B. burgdorferi antibody repertoire accounted for the obs

36 ariant antigens will become nonprotective as B. burgdorferi infection progresses.

37 is Review, we summarize interactions between B. burgdorferi and I. scapularis during infection, as we

38 sights into the complex interactions between B. burgdorferi and its arthropod vector and suggest addi

39 We showed that MBL is capable of binding B. burgdorferi through its carbohydrate recognition doma

40 protein (dbpBA) by utilizing bioluminescent B. burgdorferi reporter strains and in vivo imaging.

41 CHB probe could detect Borrelia burgdorferi (B. burgdorferi) recA gene with a sensitivity of 100 copi

42 nd compared this to the response elicited by B. burgdorferi.

43 A recombinant protein encoded by B. burgdorferi BB0723 (a putative cyaB homolog) was show

44 Induction of type I and type III IFNs by B. burgdorferi RNA could be completely abrogated by a TL

45 nfed tick or any other stage of infection by B. burgdorferi.

46 tion concepts center on proteins produced by B. burgdorferi during tick transit and on tick proteins

47 esults demonstrate that Lon-1 is required by B. burgdorferi to infect animal hosts and to cope with e

48 ole make clear that environmental sensing by B. burgdorferi directly or indirectly drives an extensiv

49 ation of small molecule inhibitors to combat B. burgdorferi infection.

50 ction may provide novel strategies to combat B. burgdorferi infection.

51 ducts BB0406 and BB0405, members of a common B. burgdorferi paralogous gene family, share 59% similar

52 In contrast, B. burgdorferi loads in distant tissue such as heart, jo

53 nfection provides new insights into critical B. burgdorferi interactions with the host required for i

54 Cultured B. burgdorferi that were genetically manipulated to prod

55 to bone marrow macrophage cultures decreased B. burgdorferi-induced TNF-alpha and KC and increased IL

56 ry transcriptional framework for delineating B. burgdorferi regulatory pathways throughout the enzoot

57 antibodies against a prototypic T-dependent B. burgdorferi protein, Arthritis-related protein (Arp),

58 ssay was successfully demonstrated to detect B. burgdorferi DNA extracted from tick species, showing

59 in whole blood samples and is able to detect B. burgdorferi in clinical samples.

60 T2MR detected B. burgdorferi in blood samples from 17/54 (31%) of pati

61 Dogmatically, B. burgdorferi can establish a persistent infection in t

62 expression both in vitro and in vivo during B. burgdorferi infection.

63 D4(+) T cells existing prior to, and during, B. burgdorferi infection have not been well characterize

64 red to two-tiered testing in detecting early B. burgdorferi infection indicates that multiplex analys

65 The deletion of bba33 eliminated B. burgdorferi infectivity in C3H mice, which was rescue

66 Molecular mechanisms that enable B. burgdorferi to detect, channel, and respond to these

67 IGTPase knockdown enhanced B. burgdorferi levels in post-fed ticks, suggesting this

68 n disulfide isomerase A3 (IsPDIA3), enhances B. burgdorferi colonization of the tick gut.

69 ates the tick gut microbiota and facilitates B. burgdorferi colonization.

70 cade, we hypothesized that BBA33 facilitates B. burgdorferi infection in the mammalian host.

71 also begins to define the genetic basis for B. burgdorferi expansion in the skin during localized in

72 ce was required along with that of bbb22 for B. burgdorferi to achieve maximal spirochete loads in in

73 weeks postinoculation and to be critical for B. burgdorferi infection of mouse hearts.

74 oth genes, bbb22 and bbb23, are critical for B. burgdorferi to achieve wild-type infection of mice an

75 sults demonstrate that Lon-2 is critical for B. burgdorferi to establish infection and to cope with e

76 The bbb23 gene was dispensable for B. burgdorferi mouse infectivity, yet its presence was r

77 the gene encoding RNase Y, is essential for B. burgdorferi growth, while ssrS, the gene encoding 6S

78 code purine permeases that are essential for B. burgdorferi mouse infectivity.

79 dependent adenine transport is essential for B. burgdorferi survival in mice.

80 these data show that BB0345 is essential for B. burgdorferi survival in the mammalian host, potential

81 We report here that DksA is essential for B. burgdorferi to infect a mammalian host.

82 tion, suggesting that Lon-2 is important for B. burgdorferi infection.

83 erstanding of factors that are important for B. burgdorferi persistence in the tick.

84 tively high level of saturation observed for B. burgdorferi PC, as vesicles containing ACGal and PC,

85 rry stain, immunohistochemistry, and PCR for B. burgdorferi, and immunohistochemistry for complement

86 f infected animals were culture positive for B. burgdorferi regardless of treatment.

87 OspC is required for B. burgdorferi to establish infection in both immunocomp

88 VlsE is required for B. burgdorferi to establish persistent infection by cont

89 Dogs are routinely screened for B. burgdorferi, but it is unknown if infection with TBRF

90 744 (also known as p83/100) by screening for B. burgdorferi strain B31 proteins that bind to alpha1be

91 c and nucleic acid amplification testing for B. burgdorferi and other tick-borne pathogens.

92 can cross-react with C6 antigen testing for B. burgdorferi, the causative agent of Lyme disease, und

93 study, we solved the structure of DbpA from B. burgdorferi strain 297 using X-ray crystallography an

94 ures demonstrated that T cells isolated from B. burgdorferi-infected but not B. burgdorferi-immunized

95 globulin genes were immunized with OspA from B. burgdorferi to generate human monoclonal antibodies (

96 the need to critically evaluate results from B. burgdorferi diagnostic tests in the context of the as

97 ssociated protein fraction of in vitro-grown B. burgdorferi.

98 dies also cross-protect against heterologous B. burgdorferi spirochetes and significantly reduce the

99 ected to secondary challenge by heterologous B. burgdorferi at different time points postinfection (p

100 deficient mice harbored significantly higher B. burgdorferi numbers in skin tissue during the early c

101 To assess the ability of homologous B. burgdorferi clones to successfully superinfect a mous

102 s transit between ticks and mammalian hosts, B. burgdorferi must dramatically alter its outer surface

103 rrelia burgdorferi Here, we investigated how B. burgdorferi exploits Fn to interact with endothelia u

104 A better understanding of how B. burgdorferi transmigrates through dermal and tissue v

105 Similar to infection of humans, B. burgdorferi establishes long-term infection in variou

106 Previously identified B. burgdorferi proteins, lipid immunogens, and live muta

107 technology (IVET)-based approach to identify B. burgdorferi genes expressed in vivo, we discovered th

108 anaging its microbiome, and how this impacts B. burgdorferi colonization of its arthropod vector.

109 However, the function of Lon-1 in B. burgdorferi biology remains virtually unknown.

110 ated function of BosR as an autoregulator in B. burgdorferi.

111 sought to investigate the role of bb0318 in B. burgdorferi pathogenesis.

112 ablished that the regulator BosR (BB0647) in B. burgdorferi plays important roles in modulating borre

113 milar under the aforementioned conditions in B. burgdorferi Among several polyamines and polyamine pr

114 stic insight into transcriptional control in B. burgdorferi, and address sigma factor function and sp

115 how bosR expression itself is controlled in B. burgdorferi remains largely unknown.

116 hat BosR may influence its own expression in B. burgdorferi However, direct experimental evidence sup

117 vestigation revealed that bosR expression in B. burgdorferi is influenced by environmental stimuli, s

118 factors exert control of gene expression in B. burgdorferi required for the completion of its enzoot

119 is of major regulators of gene expression in B. burgdorferi, such as RpoS and BosR, with a concomitan

120 interplay of multiple regulatory factors in B. burgdorferi gene expression.

121 l, principles of ordered-domain formation in B. burgdorferi appear to be very similar to those in euk

122 e of the first regulatory RNAs identified in B. burgdorferi that controls the expression of lipoprote

123 agellar assembly, morphology and motility in B. burgdorferi, but also unveils mechanistic insights in

124 report that multiple pathways participate in B. burgdorferi internalization and that different cell s

125 gnaling pathways as ones that participate in B. burgdorferi phagocytosis and the resulting cytokine a

126 l cell surface receptors that participate in B. burgdorferi phagocytosis have been reported, includin

127 the mechanisms underlying gene regulation in B. burgdorferi has been the lack of a functional assay t

128 been determined to be a master regulator in B. burgdorferi.

129 from activation of the stringent response in B. burgdorferi may also be involved in the recently desc

130 ar number and polarity; however, its role in B. burgdorferi remains unknown.

131 ously identified RpoD consensus sequences in B. burgdorferi.

132 s here the future of evolutionary studies in B. burgdorferi, focusing on the primary evolutionary for

133 is is the first comprehensive map of TSSs in B. burgdorferi and characterization of previously un-ann

134 On infection, B. burgdorferi induces selected tick proteins that modul

135 Deletion of bb0238 in infectious B. burgdorferi did not affect microbial growth in vitro

136 c csrA mutants in two widely used infectious B. burgdorferi strains.

137 including Dae2, previously shown to inhibit B. burgdorferi.

138 delines predated a full understanding of key B. burgdorferi antigens and have a number of shortcoming

139 mercial and veterinary diagnostic laboratory B. burgdorferi-based tests.

140 s role in protecting invading pathogens like B. burgdorferi.

141 BpuR bound to sodA mRNA in live B. burgdorferi, and a specific BpuR-binding site was map

142 that were inoculated intrathecally with live B. burgdorferi and either treated with dexamethasone or

143 demonstrate the detection of ospA, the major B. burgdorferi lipoprotein at the level of 4.0 fmol of o

144 formed in vitro describing the roles of many B. burgdorferi outer surface proteins in adhesion to hos

145 used both wild-type and genetically modified B. burgdorferi s. l. bacteria, recombinant borrelia adhe

146 f patients, we directly detected one or more B. burgdorferi genotypes in the skin.

147 Mutant B. burgdorferi isolates producing BB0238 lacking the 11-

148 (qPCR) demonstrated that Deltabb0744 mutant B. burgdorferi bacteria were attenuated in the ability t

149 g that the defect seen in Deltabb0744 mutant B. burgdorferi was due to the loss of BB0744.

150 oint tissue infected with Deltabb0744 mutant B. burgdorferi.

151 solated from B. burgdorferi-infected but not B. burgdorferi-immunized mice supported the rapid differ

152 against PIXR in mice, impairs the ability of B. burgdorferi to colonize the tick gut.

153 larly in heart tissue, alters the ability of B. burgdorferi to disseminate efficiently, or both.

154 of LD is mainly attributed to the ability of B. burgdorferi to persist in patients for many years des

155 Two-dimensional electrophoresis analysis of B. burgdorferi B31A3 and a strain that overexpresses Htr

156 Through a detailed analysis of B. burgdorferi infection kinetics, we discovered that bb

157 Injection of AC directly into the ankles of B. burgdorferi-infected mice limited ankle swelling but

158 bb0345 of B. burgdorferi encodes a hypothetical protein of unknown

159 ditions not yet identified or that BB0449 of B. burgdorferi has a function other than ribosome confor

160 olesterol could enhance the organ burdens of B. burgdorferi and the spirochetemia of B. hispanica in

161 Since the clearance of B. burgdorferi is mediated by humoral immunity in NZW ra

162 by which MBL facilitates early clearance of B. burgdorferi.

163 showed that HtrA and p66 are constituents of B. burgdorferi outer membrane vesicles.

164 se CD4 T cells contributed to the control of B. burgdorferi burden and supported the induction of B.

165 osR throughout the tick-mammal life cycle of B. burgdorferi via quantitative reverse transcription (R

166 ions and show promise in direct detection of B. burgdorferi infections.

167 w approach was first applied to detection of B. burgdorferi membrane proteins supplemented in human s

168 Our results indicated that detection of B. burgdorferi membrane proteins, which are approximatel

169 ophysical model for the swimming dynamics of B. burgdorferi suggested that cell speed should increase

170 ion could potentially explain the failure of B. burgdorferi to persist.

171 tick colonization, we constructed a form of B. burgdorferi in which the ospA open reading frame, on

172 evaluate the induction and functionality of B. burgdorferi infection-induced CD4 T(FH) cells.

173 not associated with a particular genotype of B. burgdorferi.

174 ettsii The sensitivity for identification of B. burgdorferi was 44.4% compared to a composite gold st

175 Live imaging of B. burgdorferi caught in the act of being acquired revea

176 orferi burden and supported the induction of B. burgdorferi-specific IgG responses.

177 1 plays a critical role for the infection of B. burgdorferi in a mammalian host.

178 an in vivo model of vascular interaction of B. burgdorferi in which the bacteria are injected intrav

179 the number of AC increases in the joints of B. burgdorferi-infected mice around day 21 postinfection

180 zone directly into the tibiotarsal joints of B. burgdorferi-infected mice decreased ankle swelling an

181 tical traps to bend unflagellated mutants of B. burgdorferi.

182 tion site was followed by reduced numbers of B. burgdorferi spirochetes in the bloodstream and, ultim

183 play important roles in the pathogenesis of B. burgdorferi that extend beyond its transport function

184 t role in the chemotaxis and pathogenesis of B. burgdorferi We propose potential connections between

185 terol levels can affect the pathogenicity of B. burgdorferi.

186 In addition, phagocytosis of B. burgdorferi and neutrophil migration to LTB(4) were i

187 ission, survival and pathogenic potential of B. burgdorferi depend on the bacterium's ability to modu

188 0744 that alters the pathogenic potential of B. burgdorferi.

189 rn Hemispheres, evidence for the presence of B. burgdorferi s.l. in South America apart from Uruguay

190 udies reveal that HtrA, a serine protease of B. burgdorferi, controls FlaB turnover.

191 estingly, FlaB, a major flagellin protein of B. burgdorferi, is degraded in the fliD mutant but not i

192 spatiotemporal transcriptional regulation of B. burgdorferi during mammalian infection of borrelial o

193 e required for enhancing serum resistance of B. burgdorferi in vitro.

194 e bb0318 in the oxidative stress response of B. burgdorferi and indicate the contribution of bb0318 t

195 vivo model to define the biological roles of B. burgdorferi adhesins in tissue-specific vascular inte

196 data also suggest that the helical shape of B. burgdorferi itself, providing sites of high curvature

197 population fluctuations and/or stability of B. burgdorferi s.l. in these habitats.

198 rotective role of MBL in the early stages of B. burgdorferi infection, yet the underlying mechanism w

199 The genotype of the infecting strain of B. burgdorferi was evaluated in subjects with PTLDS.

200 ctional impairment or a particular strain of B. burgdorferi.

201 ing antimicrobial treatment, both strains of B. burgdorferi, N40 and B31, lose one or more plasmids.

202 t contribute to colonization and survival of B. burgdorferi in the mammalian host.

203 rrelia burgdorferi The long-term survival of B. burgdorferi spirochetes in the mammalian host is achi

204 the role of trained immunity on symptoms of B. burgdorferi infection may provide insight into the pa

205 ld gel electrophoresis differed from that of B. burgdorferi B31A3.

206 lobally identify the 5' end transcriptome of B. burgdorferi grown in culture as a means to validate n

207 urine model of tick-mediated transmission of B. burgdorferi CONCLUSIONS: Our study indicates that Osp

208 or mammalian infectivity and transmission of B. burgdorferi.

209 e host immunity blocking the transmission of B. burgdorferi.

210 that reported round morphologic variants of B. burgdorferi in specimens obtained from 32 total patie

211 ince motility is crucial to the virulence of B. burgdorferi, the results suggest that sublethal doses

212 al anesthetic used for human skin biopsy, on B. burgdorferi presence was measured.

213 onization of the tick gut after engorging on B. burgdorferi-infected mice.

214 Ixodes ticks parasitizing B. burgdorferi-infected mice upregulated an I. scapulari

215 ant B6 mice and not unique to any particular B. burgdorferi strain.

216 log phase and 7-10 days old stationary phase B. burgdorferi.

217 ombined data demonstrate that DksA regulates B. burgdorferi virulence at least partially through its

218 59% similarity and are grouped into the same B. burgdorferi paralogous gene family.

219 led, as did attempts to amplify and sequence B. burgdorferi from the five individual samples comprisi

220 In this study, B. burgdorferi-negative dogs were inoculated with B. tur

221 clone in order to distinguish superinfecting B. burgdorferi from primary-infecting spirochetes.

222 MP (c-di-GMP) synthesis by the Hk1/Rrp1 TCS; B. burgdorferi lacking either component is destroyed dur

223 ) and CD8(+) T cells to a larger extent than B. burgdorferi.

224 reater capacity to survive tick feeding than B. burgdorferi Deltahk1 or Deltarrp1 mutants, establishi

225 Here, we demonstrate that B. burgdorferi controls transcription of bpuR, expressin

226 These finding demonstrate that B. burgdorferi engages unknown genetic mechanisms to uni

227 We demonstrate that B. burgdorferi N40 needle-infected C57BL/6 MBL deficient

228 Earlier studies demonstrated that B. burgdorferi synthesizes 4,5-dihydroxy-2,3-pentanedion

229 Furthermore, our finding that B. burgdorferi sheds immunogenic PG(Bb) fragments during

230 We found that B. burgdorferi does not primarily target insoluble matri

231 Bioinformatic analyses indicate that B. burgdorferi harbors an hpf homolog, the bb0449 gene.

232 Our biochemical analysis indicates that B. burgdorferi CheD significantly enhances CheX phosphat

233 The observation that B. burgdorferi contains a TamB ortholog that interacts w

234 These results show that B. burgdorferi can transform a ubiquitous but normally n

235 Here we show that B. burgdorferi colonization increases the expression of

236 We show that B. burgdorferi has a chemically atypical PG (PG(Bb)) tha

237 Animal models have shown that B. burgdorferi persists in the skin.

238 The data further suggest that B. burgdorferi infection drives the humoral response awa

239 een infected multiple times, suggesting that B. burgdorferi exposure may elicit strain-specific immun

240 The B. burgdorferi-infected patient presented with fever, wh

241 As the B. burgdorferi infection further progressed, however, re

242 To begin to characterize the B. burgdorferi transcriptome during murine infection, we

243 Here, we systematically characterized the B. burgdorferi CheD homolog using genetics and biochemic

244 lification-microarray approach to define the B. burgdorferi transcriptomes in fed larvae, fed nymphs

245 ability to regulate events critical for the B. burgdorferi enzootic cycle.

246 Further, the B. burgdorferi sensu stricto-infected KO mice had persis

247 In a head-to-head comparison, however, the B. burgdorferi Deltaglp mutant had a markedly greater ca

248 peptidoglycan (PG), a major component of the B. burgdorferi cell envelope, may contribute to the deve

249 ds another layer to our understanding of the B. burgdorferi regulome, and provides further evidence t

250 Borrelia garinii, a member of the B. burgdorferi s. l. complex, adhered to biglycan expres

251 Previous studies determined that the B. burgdorferi BpuR protein binds to its own mRNA and au

252 However, our recent study has shown that the B. burgdorferi spirochete is effectively cleared by anti

253 ed an in vitro transcription assay using the B. burgdorferi RNA polymerase holoenzyme.

254 Therefore, B. burgdorferi was not confirmed in any sample.

255 mong uninfected I. scapularis nymphal ticks, B. burgdorferi-infected nymphal ticks and B. mayonii-inf

256 Particularly, the contribution of Lon-1 to B. burgdorferi fitness and infection remains hitherto un

257 To date, the contribution of Lon-2 to B. burgdorferi fitness and infection remains unexplored.

258 tect intrathecal production of antibodies to B. burgdorferi is the antibody index assay, which correc

259 r the detection of IgM and IgG antibodies to B. burgdorferi The BioPlex 2200 Lyme Total assay exhibit

260 g performance for detection of antibodies to B. burgdorferi using the PPO triplex test (rP100 + PepVF

261 over, administration of IsPDIA3 antiserum to B. burgdorferi-infected mice reduced the ability of spir

262 i and indicate the contribution of bb0318 to B. burgdorferi mammalian infectivity.

263 ts and their transport systems contribute to B. burgdorferi adaptation during the vector and vertebra

264 ly, it was reported that CsrA contributes to B. burgdorferi infectivity and is required for the activ

265 and/or translation of genes contributing to B. burgdorferi infectivity.

266 To date, the contribution of DksA to B. burgdorferi infection remains unknown.

267 d PCR and serologic evidence for exposure to B. burgdorferi could be differentiated as a group from P

268 years, suggesting that previous exposure to B. burgdorferi may not elicit a protective immune respon

269 Although adaptive immunity to B. burgdorferi has been extensively characterized, consi

270 residues in these two motifs were lethal to B. burgdorferi.

271 of the contribution of the genes on lp36 to B. burgdorferi infection but also begins to define the g

272 nflammatory cytokines in a similar manner to B. burgdorferi.

273 esence of intrathecal antibody production to B. burgdorferi and therefore should not be offered.

274 miyamotoi that is similar to the response to B. burgdorferi and is able to induce T cell proliferatio

275 it is expected that the antibody response to B. burgdorferi invariant antigens will become nonprotect

276 rotective efficacy of the immune response to B. burgdorferi surface antigens were monitored via a sup

277 the joint-specific inflammatory response to B. burgdorferi.

278 fectively kill in vitro doxycycline-tolerant B. burgdorferi.

279 xime effectively killed doxycycline-tolerant B. burgdorferi.

280 une pathways engaged during tick-transmitted B. burgdorferi infection would further development of va

281 that azlocillin can be effective in treating B. burgdorferi sensu stricto JLB31 infection and further

282 etectable spirochetemia induced by wild-type B. burgdorferi (WT), indicating that VlsE was likely the

283 conditions, the swimming speed of wild-type B. burgdorferi slowed by approximately 15%, with only ma

284 significantly higher than parental wild-type B. burgdorferi strains, suggesting that OspC has an anti

285 In wild-type B. burgdorferi, bb0449 transcript and BB0449 protein lev

286 ave provided additional evidence that viable B. burgdorferi do not persist after conventional treatme

287 Interestingly, mixtures of ACGal with B. burgdorferi PC formed ordered domains more readily th

288 ouse strain, C3H/HeN develops arthritis with B. burgdorferi infection whereas another strain, C57BL/6

289 s, and humans indicate that coinfection with B. burgdorferi and B. microti is common, promotes transm

290 nstream of these receptors upon contact with B. burgdorferi We identified both Syk and Src signaling

291 sociated cytokines, correlated directly with B. burgdorferi immunoglobulin G antibodies (P </= .02),

292 3H and C3H BLT1(-/-) mice were infected with B. burgdorferi and arthritis progression was monitored b

293 apoE- and LDLR-deficient mice infected with B. burgdorferi had an increased number of spirochetes in

294 t (C57BL/6 [B6]) mouse strains infected with B. burgdorferi strains N40 and B31 and to confirm the ge

295 pts to demonstrate persistent infection with B. burgdorferi has not been established.

296 f regulatory T cells prior to infection with B. burgdorferi resulted in sustained swelling, as well a

297 nally, infection of AP-3-deficient mice with B. burgdorferi resulted in altered joint inflammation du

298 disease following infection of C3H mice with B. burgdorferi.

299 ents produces antibodies cross-reactive with B. burgdorferi assays.

300 e marrow-derived macrophages stimulated with B. burgdorferi, and it was responsible for feed-forward