ライフサイエンスコーパス: B. burgdorferi

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

2 B. burgdorferi appears to lack the metabolic capacity fo

3 B. burgdorferi can utilize glycerol as a carbohydrate so

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

5 B. burgdorferi clones containing point mutations in cons

6 B. burgdorferi elongates from discrete zones that are bo

7 B. burgdorferi is known to be unique in metal utilizatio

8 B. burgdorferi isolates were cultivated in Barbour-Stoen

9 B. burgdorferi regulates gene expression in response to

10 B. burgdorferi SodA shows strong overall homology with o

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

12 B. burgdorferi was weakly amplified from one pool using

13 B. burgdorferi's periplasmic flagellar filaments are com

14 B. burgdorferi-infected mice were subjected to secondary

15 g sites have been identified upstream of 156 B. burgdorferi genes.

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

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

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

19 we utilized targeted deletion to generate a B. burgdorferi clone that lacked only the arp gene locus

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

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

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

23 Autophagy induction against B. burgdorferi was dependent on reactive oxygen species

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

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

26 nd domain swapping between the S. aureus and B. burgdorferi proteins identified that a 6-residue stre

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

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

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

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

31 he first evidence that, by utilizing BbHtrA, B. burgdorferi may actively participate in its dissemina

32 Here we describe a novel interaction between B. burgdorferi and the major ECM proteoglycan found in j

33 ur understanding of the interactions between B. burgdorferi and its murine host in the establishment

34 or this process, despite its ability to bind B. burgdorferi peptidoglycan.

35 Nevertheless, DNA was detected by B. burgdorferi-specific PCR for up to 56 days in aliquot

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

37 FN-alpha and IFN-lambda1, a type III IFN, by B. burgdorferi RNA or live spirochetes required TLR7-dep

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

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

40 early and persistent mammalian infection by B. burgdorferi.

41 ammalian infectious processes carried out by B. burgdorferi.

42 h, in turn, modulates cytokine production by B. burgdorferi for the first time.

43 ermined that OspC production was required by B. burgdorferi throughout SCID mouse infection if the vl

44 ups of pathogens represented respectively by B. burgdorferi, the agent of Lyme borreliosis, and B. he

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

46 ch mitochondria of Saccharomyces cerevisiae, B. burgdorferi SodA was inactive.

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

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

49 However, neither of the complemented B. burgdorferi strains was capable of persisting through

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

51 badR-deficient B. burgdorferi were unable to colonize mice.

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

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

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

55 udy attempted to use xenodiagnosis to detect B. burgdorferi in patients who have been treated for Lym

56 qPCR analyses of unfed nymphs detected B. burgdorferi genomes in several nymphs at low copy num

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

58 on of the cytokine response generated during B. burgdorferi infection.

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

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

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

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

63 We recently reported that a surface-exposed B. burgdorferi protease, which is expressed during human

64 e (MSCRAMM) protein family, which facilitate B. burgdorferi adherence to extracellular matrix compone

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

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

67 lts suggest a role for BBA66 in facilitating B. burgdorferi dissemination and transmission from the t

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

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

70 gene(s) or regulatory elements critical for B. burgdorferi survival and pathogenesis in the Ixodes v

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

72 ve been found to encode factors critical for B. burgdorferi to complete the infectious cycle.

73 As BB0323 is a membrane protein crucial for B. burgdorferi survival in vivo, exploring its function

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

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

76 ) mediated by these lysines is essential for B. burgdorferi murine infection.

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

78 ty of the I. scapularis PM was essential for B. burgdorferi to efficiently colonize the gut epitheliu

79 ty of innate immunity as a driving force for B. burgdorferi heterogeneity during the enzootic cycle i

80 i-GMP (c-di-GMP), which is indispensable for B. burgdorferi to survive in the tick vector.

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

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

83 Xenodiagnosis was positive for B. burgdorferi DNA in a patient with erythema migrans ea

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

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

86 and pncA, are postulated to play a role for B. burgdorferi to infect and persist in Ixodes ticks.

87 744 (also known as p83/100) by screening for B. burgdorferi strain B31 proteins that bind to alpha1be

88 Ticks were tested for B. burgdorferi by polymerase chain reaction (PCR), cultu

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

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

91 Spleen cells obtained from B. burgdorferi-infected, "arthritis-resistant" wild-type

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

93 ned the mature P66 amino acid sequences from B. burgdorferi and B. garinii, we found that K487 was pr

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

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

96 Superinfection by heterologous B. burgdorferi strains has been established experimental

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

98 mentally, although the ability of homologous B. burgdorferi clones to superinfect a host has not been

99 data demonstrate an inability of homologous B. burgdorferi to superinfect immunocompetent mice as op

100 ypes of immunodeficient mice with homologous B. burgdorferi indicate that the murine innate immune sy

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

102 This reveals the molecular basis for how B. burgdorferi evades innate immunity and suggests how O

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

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

105 In addition to type I and type III IFNs, B. burgdorferi RNA contributed to the production of the

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

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

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

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

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

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

112 questions concerning the function of CsrA in B. burgdorferi gene regulation remain unanswered.

113 a first step in characterizing mRNA decay in B. burgdorferi and in investigating its role in gene exp

114 In this study, we monitored mRNA decay in B. burgdorferi following transcriptional arrest with act

115 BadR levels are elevated in B. burgdorferi cultures grown under in vitro conditions

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

119 Bb that regulate adaptive gene expression in B. burgdorferi.

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 the role of biologically available metals in B. burgdorferi.

123 ng and histopathological changes observed in B. burgdorferi-infected, IL-10-deficient mice.

124 ng that P66 associates with OspA and OspB in B. burgdorferi.

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

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

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

128 CsrA may influence the RpoN-RpoS pathway in B. burgdorferi.

129 fied a periplasmic BB0323 binding protein in B. burgdorferi, annotated as BB0104, having serine prote

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

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

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

133 ering an inducible csrA expression system in B. burgdorferi, controlled hyperexpression of CsrA in a

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

135 (c-di-GMP), governs glycerol utilization in B. burgdorferi.

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

137 yD88 were infected with a pool of infectious B. burgdorferi transposon mutants with insertions in the

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

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

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

141 that BpaB binds erp, ssbP, and nucP in live B. burgdorferi.

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 Many B. burgdorferi surface lipoproteins fall into two distin

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

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

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 Analyses of B. burgdorferi gene expression in mouse tissues showed c

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

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

157 omic approach, we demonstrate that a bulk of B. burgdorferi SodA directly associates with manganese,

158 lains a large increase in pathogen burden of B. burgdorferi in the joint of iNKT cell-deficient mice,

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

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

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

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

163 onsidering the unique enzootic life cycle of B. burgdorferi, it is not surprising that a large propor

164 for motility in the mouse-tick life cycle of B. burgdorferi.

165 d OAS1 were induced by endosomal delivery of B. burgdorferi DNA, RNA, or whole-cell lysate, but not b

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

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

168 d play a beneficial role in dissemination of B. burgdorferi in the human host and may possibly aid th

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

170 immunity in limiting early establishment of B. burgdorferi infection.

171 genome analysis has revealed a new family of B. burgdorferi proteins containing the von Willebrand fa

172 not essential, contribute to the fitness of B. burgdorferi during infection.

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

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

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

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

177 ugh the dermis, suggesting the importance of B. burgdorferi motility in evading host clearance.

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

179 The infectivity of B. burgdorferi expressing individual dbpA lysine point m

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

181 is illuminating mechanisms of interaction of B. burgdorferi with the host and the importance of multi

182 nockdown ticks, results in reduced levels of B. burgdorferi persistence within ticks.

183 re-forming activity in the outer membrane of B. burgdorferi.

184 nal studies that described the morphology of B. burgdorferi from patients with Lyme disease, the orga

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

186 Few membrane-spanning OMPs of B. burgdorferi have been definitively identified, and no

187 The outer surface protein E (OspE) of B. burgdorferi is needed for this because it recruits co

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

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

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

191 Successful penetrance of B. burgdorferi out of the vasculature and into the joint

192 itor the composition of mixed populations of B. burgdorferi during infection.

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

194 0744 that alters the pathogenic potential of B. burgdorferi.

195 In addition, the presence of B. burgdorferi DNA and mRNA was assayed by PCR and by re

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

197 The unique properties of B. burgdorferi SodA may represent adaptation to expressi

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

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

200 nd in modulating the chemotactic response of B. burgdorferi.

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

202 We show here that the swimming speeds of B. burgdorferi and T. pallidum decrease with increases i

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

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

205 were due to the same or different strains of B. burgdorferi.

206 d the loop containing K487 on the surface of B. burgdorferi.

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

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

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

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

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

212 The transmission of B. burgdorferi to humans can be disrupted by targeting 2

213 or mammalian infectivity and transmission of B. burgdorferi.

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

215 chbC encodes a key chitobiose transporter of B. burgdorferi.

216 literature to justify specific treatment of B. burgdorferi morphologic variants.

217 udies in which round morphologic variants of B. burgdorferi have been described in situ in human spec

218 a pathogenic role to morphologic variants of B. burgdorferi in either typical manifestations of Lyme

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

220 Viability of B. burgdorferi was assessed by subculture, growth, morph

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

222 in carbohydrate utilization and virulence of B. burgdorferi.

223 . scapularis larvae for the xenodiagnosis of B. burgdorferi infection in humans.

224 arate evaluation of each factor's impacts on B. burgdorferi gene and protein expression.

225 each strain were treated with trypsin, only B. burgdorferi P66 was trypsin sensitive, indicating tha

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

227 59% similarity and are grouped into the same B. burgdorferi paralogous gene family.

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

229 y other investigators suggested that several B. burgdorferi lipoproteins, including OspA and VlsE, co

230 Upon infection, some B. burgdorferi genes are upregulated, including members

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

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

233 d a quantitative trait locus on Chr4, termed B. burgdorferi-associated locus 1 (Bbaa1), that regulate

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

235 These data demonstrate that B. burgdorferi possess aggrecan-binding proteins which m

236 These studies demonstrated that B. burgdorferi infection induced type I interferon recep

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

238 our studies provide the first evidence that B. burgdorferi possess proteolytic activity which may co

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

240 Not only is iron low, but we show here that B. burgdorferi has the capacity to accumulate remarkably

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

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

243 e findings further reinforce the notion that B. burgdorferi utilizes its limited signaling systems an

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

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

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

247 We also show that B. burgdorferi is able to penetrate matrices with pore s

248 Taken together, the results suggest that B. burgdorferi DNA and mRNA can be detected in samples l

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

250 These results suggest that B. burgdorferi viability is rapidly eliminated after ant

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

252 We demonstrate that DNA and RNA are the B. burgdorferi components that initiate a type I IFN res

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

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

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

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

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

258 forming activity, forms a beta-barrel in the B. burgdorferi OM.

259 , we found that K487 was present only in the B. burgdorferi P66 protein sequence.

260 burgdorferi and that autophagy modulates the B. burgdorferi-dependent cytokine production.

261 ed from the mice and the compositions of the B. burgdorferi populations at the injection site and in

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

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

264 Thus, B. burgdorferi infection drives the production of type I

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

266 e contribution of genes carried by lp28-3 to B. burgdorferi infection.

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

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

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

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

271 me the induction of autophagy by exposure to B. burgdorferi and that autophagy modulates the B. burgd

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

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

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

275 ing activities of this OMP as they relate to B. burgdorferi physiology and Lyme disease pathogenesis.

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

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

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

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

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

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

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

283 l transmission relative to that of wild-type B. burgdorferi.

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

285 ies continue to provide evidence that viable B. burgdorferi do not persist in patients who receive co

286 Whereas B. burgdorferi SodA has evolved in a manganese-rich, iro

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

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

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

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

291 ting SWNT FETs was seen upon incubation with B. burgdorferi flagellar antigen, indicative of the nano

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

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

294 rized, and their roles during infection with B. burgdorferi have not been elucidated.

295 sult in diminished control of infection with B. burgdorferi in a murine model of disease.

296 These iNKT cells interacted with B. burgdorferi at the vessel wall and disrupted dissemin

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

300 t amount of IL-17 following stimulation with B. burgdorferi.