ライフサイエンスコーパス: H. ducreyi

1 H. ducreyi 35000HP produced AI-2 that functioned in a Vi

2 H. ducreyi 35000HP-SMS4 and its parent, 35000HP, had sim

3 H. ducreyi activated NK cells only in the presence of an

4 H. ducreyi also harbors a homologue of RpoE, which is th

5 H. ducreyi colocalized with collagen and fibrin but not

6 H. ducreyi contains two genes, lspA1 and lspA2, which en

7 H. ducreyi culture supernatant and H. ducreyi lipooligos

8 H. ducreyi does not synthesize sialic acid, which must b

9 H. ducreyi evades uptake by polymorphonuclear leukocyte

10 H. ducreyi serum resistance protein A (DsrA) is a member

11 H. ducreyi upregulated few genes (hgbA, flp-tad, and lsp

12 H. ducreyi was associated with polymorphonuclear leukocy

13 H. ducreyi was observed as individual cells and in clump

14 H. ducreyi was recovered at biopsy from 6 of 7 parent si

15 H. ducreyi was recovered from six of seven biopsied pare

16 H. ducreyi-infected monocytes and monocyte-derived macro

17 bility, we examined sequence diversity at 11 H. ducreyi loci, including virulence and housekeeping ge

18 DNA microarray analysis revealed that 324 H. ducreyi genes were differentially regulated after gro

19 A H. ducreyi cpxR mutant was compared with its parent for

20 A H. ducreyi luxS mutant was constructed by insertional in

21 ncode a sialyltransferase, we complemented a H. ducreyi lst mutant with cpsK.

22 sapA mutant, the sapBC mutant did not affect H. ducreyi's resistance to human defensins.

23 splayed enhanced phagocytic activity against H. ducreyi and similar bacterial killing.

24 All H. ducreyi strains were positive, and all other bacteria

25 Although H. ducreyi is predominantly extracellular during human i

26 We found that although H. ducreyi strain 35000 adhered efficiently to U-937 cel

27 An H. ducreyi mutant with an inactivated tadA gene exhibite

28 An H. ducreyi strain lacking the ncaA gene was impaired in

29 to the HgbA vaccine is protective against an H. ducreyi infection, possibly by preventing acquisition

30 Here, we compared an H. ducreyi neuA mutant to its wild-type parent in severa

31 Here, we constructed an H. ducreyi dksA mutant and showed it was also partially

32 We discovered an H. ducreyi outer membrane protein required for expressio

33 From an H. ducreyi 35000HP genomic DNA library, a clone compleme

34 rial sialyltransferases; LOS derived from an H. ducreyi CMP-Neu5Ac synthetase (neuA) mutant has no de

35 However, an H. ducreyi sialyltransferase (lst) mutant, whose LOS con

36 onectin and conferred serum resistance to an H. ducreyi serum-sensitive strain.

37 that sapA is expressed in broth cultures and H. ducreyi-infected tissue; sapA is also conserved among

38 ere, we examined interactions between DC and H. ducreyi 35000HP, which produces LspA1, LspA2, and CDT

39 es of H. somnus 129Pt, H. influenzae Rd, and H. ducreyi 35000HP revealed similarities and differences

40 9 genital ulcer specimens, respectively, and H. ducreyi DNA was detected in 60% (3 of 5) of samples f

41 H. ducreyi culture supernatant and H. ducreyi lipooligosaccharides (LOS) induced IDO expres

42 for experimental chancroid, whereas another H. ducreyi mutant with inactivated flp-1 and flp-2 genes

43 By dual staining with polyclonal anti-H. ducreyi antiserum and MAbs that recognize human skin

44 Sections were stained with polyclonal anti-H. ducreyi antiserum or H. ducreyi-specific monoclonal a

45 7(lo/-)FOXP3(+) T(reg) cells are expanded at H. ducreyi-infected sites and that these cells may play

46 ed to the inoculum (mid-log-phase bacteria), H. ducreyi harvested from pustules differentially expres

47 teers were experimentally infected with both H. ducreyi 35000HP and the tadA mutant, 35000HP.400.

48 Heme is acquired by H. ducreyi from its human host via TonB-dependent transp

49 h the limitation of heme/iron acquisition by H. ducreyi.

50 First, FN binding by H. ducreyi was greatly increased in bacteria grown on he

51 otein may have a minor role in FN binding by H. ducreyi, since a double dsrA momp mutant bound less F

52 nal antibody partially blocked FN binding by H. ducreyi.

53 nzymatically active IDO was induced in DC by H. ducreyi.

54 lls abrogated IL-1beta secretion elicited by H. ducreyi.

55 r both are required for pustule formation by H. ducreyi in humans.

56 ore is not required for pustule formation by H. ducreyi in humans.

57 OMP is not required for pustule formation by H. ducreyi in the human model of infection.

58 er is essential for microcolony formation by H. ducreyi, whereas this phenotypic trait is not linked

59 essary for the inhibition of phagocytosis by H. ducreyi.

60 obin is the sole source of heme/iron used by H. ducreyi in vivo and has implications for the potentia

61 required for full expression of virulence by H. ducreyi in humans but have less of a role in virulenc

62 LspA proteins in cell-free concentrated H. ducreyi culture supernatant fluid could also be tyros

63 d, under certain conditions, in concentrated H. ducreyi culture supernatant fluids that lacked detect

64 ctivity plays a critical role in controlling H. ducreyi virulence in vivo.

65 , respectively, for the diagnosis of current H. ducreyi infection.

66 ype parent strain and a previously described H. ducreyi cdtC mutant to determine the relative contrib

67 sensitivity may not be sufficient to detect H. ducreyi in all clinical specimens, further work to in

68 es two outer membrane proteins, called DltA (H. ducreyi lectin A) and DsrA (H. ducreyi serum resistan

69 called DltA (H. ducreyi lectin A) and DsrA (H. ducreyi serum resistance A), that contribute to the a

70 fficking to skin in response to experimental H. ducreyi infection.

71 Escherichia coli expressing H. ducreyi NcaA bound to type I collagen, demonstrating

72 35000HPDeltacpxA is the first H. ducreyi mutant that is impaired in its ability to for

73 rient stress and anaerobiosis is crucial for H. ducreyi survival in humans.

74 nd OmpP2B are the first porins described for H. ducreyi.

75 t that sialylation of LOS is dispensable for H. ducreyi pathogenesis in humans.

76 outer membrane protein that is important for H. ducreyi collagen binding and host colonization.

77 rting the finding that fgbA is important for H. ducreyi infection.

78 ted carbohydrates (CHO) and is important for H. ducreyi serum resistance.

79 a virulence factor and as one mechanism for H. ducreyi to resist killing by antimicrobial peptides.

80 stem that has been shown to be necessary for H. ducreyi to inhibit phagocytosis by immune cells in vi

81 Expression of HgbA is necessary for H. ducreyi to survive and initiate disease in a human mo

82 CdtA, CdtB, and CdtC appeared necessary for H. ducreyi-derived culture supernatant fluid to exhibit

83 th the ncaA mutant were culture positive for H. ducreyi 7 days after inoculation, compared to 73% of

84 ollagen binding protein NcaA is required for H. ducreyi infection.

85 -kinase signaling pathways were required for H. ducreyi-induced IL-10 production in MDM.

86 We constructed an unmarked, in-frame H. ducreyi cpxA deletion mutant, 35000HPDeltacpxA.

87 Concentrated culture supernatant fluids from H. ducreyi lspB and lspA1 lspB mutants did not contain d

88 Immunodepletion of LspA proteins from H. ducreyi culture supernatant fluid abolished this inhi

89 ative hemoglobin receptor HgbA purified from H. ducreyi class I strain 35000HP (nHgbAI) and administe

90 o fulfill its obligate requirement for heme, H. ducreyi uses two TonB-dependent receptors: the hemogl

91 allenge with homologous but not heterologous H. ducreyi, suggesting that a bivalent HgbA vaccine may

92 n adhesion A), DltA (ducreyi lectin A), Hlp (H. ducreyi lipoprotein), major OMP, and/or OmpA2 (for OM

93 ent bactericidal activity against homologous H. ducreyi strain 35000HP and heterologous strain CIP542

94 rotected against a challenge from homologous H. ducreyi strain 35000HPhgbAI but not heterologous stra

95 However, how H. ducreyi transcriptionally responds to stress during h

96 To potentially understand how H. ducreyi responds to membrane stress, here we defined

97 However, H. ducreyi does not have genes that are highly homologou

98 In humans, H. ducreyi is found in an abscess and overcomes a hostil

99 In humans, H. ducreyi is surrounded by phagocytes and must adapt to

100 In humans, H. ducreyi resides in an abscess and must adapt to a var

101 We identified H. ducreyi in 16 of 18 pustules but did not detect bacte

102 ong clinical isolates of both class I and II H. ducreyi strains, supporting the finding that fgbA is

103 DsrA proteins from both class I and class II H. ducreyi strains mediated FN and vitronectin binding.

104 so conserved among both class I and class II H. ducreyi strains.

105 gative bacteria and regulates some important H. ducreyi virulence factors.

106 We identified a 15-gene cluster in H. ducreyi that encoded predicted protein products with

107 me of the tad locus; this 15-gene cluster in H. ducreyi was designated flp.

108 cells with up-regulated HIV-1 coreceptors in H. ducreyi-infected lesions may provide an environment t

109 ltransferase gene (Hd0053) was discovered in H. ducreyi, raising the possibility that Hd0053 compensa

110 for metabolic oligosaccharide engineering in H. ducreyi and possibly other prokaryotes that share sim

111 CpsK was expressed in H. ducreyi and LOS was isolated and analysed for sialic

112 se responses, we profiled gene expression in H. ducreyi-infected and uninfected monocyte-derived DC.

113 system in regulating virulence expression in H. ducreyi.

114 tant-parent trials confirmed key features in H. ducreyi pathogenesis, and the model has provided an o

115 an operon containing two additional genes in H. ducreyi 35000HP.

116 roles in regulating envelope homeostasis in H. ducreyi.

117 sponded directly with a fivefold increase in H. ducreyi-specific antibody titers and the emergence of

118 membrane protein OmpA2 were not involved in H. ducreyi FN binding, since single mutants bound FN as

119 t of a beta-defensin resistance mechanism in H. ducreyi and shows that LL-37 resistance in H. ducreyi

120 The importance of NcaA in H. ducreyi pathogenesis was assessed using both swine an

121 els of sialylated LOS glycoforms observed in H. ducreyi are in large part controlled by the exogenous

122 ression of the serum resistance phenotype in H. ducreyi.

123 elA is the primary synthetase of (p)ppGpp in H. ducreyi.

124 mutant, FX517, was constructed previously in H. ducreyi 35000.

125 s of (p)ppGpp and DksA in gene regulation in H. ducreyi, we defined genes potentially altered by (p)p

126 Therefore, serum resistance in H. ducreyi does not require expression of full-length LO

127 . ducreyi and shows that LL-37 resistance in H. ducreyi is multifactorial.

128 required for high-level serum resistance in H. ducreyi.

129 hich also contributes to serum resistance in H. ducreyi.

130 orter in antimicrobial peptide resistance in H. ducreyi.

131 The only obvious 2CST system in H. ducreyi is CpxRA; CpxR is a response regulator, and C

132 these data suggest that the CpxRA system in H. ducreyi, in contrast to that in E. coli, may be invol

133 activation of CpxRA, the only intact TCS in H. ducreyi, does not regulate homologues of envelope pro

134 hese genes were independently transcribed in H. ducreyi 35000HP.

135 onents were transcriptionally upregulated in H. ducreyi-infected skin.

136 re, loop 6 was cleaved by protease on intact H. ducreyi, suggesting surface exposure.

137 ng this construction was electroporated into H. ducreyi 35000HP, and an isogenic MOMP-deficient mutan

138 opy both failed to demonstrate intracellular H. ducreyi.

139 We investigated H. ducreyi FN binding and report several important findi

140 Isogenic H. ducreyi cdtA and cdtB mutants were constructed and us

141 ion of Cu-Zn SOD and constructed an isogenic H. ducreyi strain with a mutation in the sodC gene (3500

142 ction of MDM with live, but not heat-killed, H. ducreyi induced caspase-1- and caspase-5-dependent pr

143 croid ulcers can persist for months and live H. ducreyi can be isolated from these lesions.

144 Many H. ducreyi strains express cytolethal distending toxin (

145 Finally, all of nine H. ducreyi strains tested were antiphagocytic, suggestin

146 These novel H. ducreyi mutants provide important tools for studying

147 nd DksA altered expression of 28% and 17% of H. ducreyi open reading frames, respectively, including

148 macrophages, we investigated the ability of H. ducreyi strain 35000 to adhere to, invade, and surviv

149 specifically responsible for the ability of H. ducreyi to bind vitronectin.

150 ession of wecA contributes to the ability of H. ducreyi to cause pustules in humans.

151 f LspA1 and LspA2 facilitates the ability of H. ducreyi to initiate disease and to progress to pustul

152 xpression of DsrA facilitates the ability of H. ducreyi to progress to the pustular stage of disease.

153 n of csrA resulted in decreased adherence of H. ducreyi to human foreskin fibroblasts (HFF); Flp1 and

154 a(v)beta(5) did not affect the attachment of H. ducreyi to HaCaT cells.

155 n and vitronectin and mediates attachment of H. ducreyi to keratinocytes.

156 To better understand the biology of H. ducreyi, we developed a human inoculation model.

157 Blockage of H. ducreyi uptake by cytochalasin D significantly reduce

158 The minimum number of CFU of H. ducreyi detected was 2 x 10(6) CFU, and the minimum a

159 The implications of two classes of H. ducreyi strains differing in important antigenic oute

160 or involved in FN binding by both classes of H. ducreyi strains.

161 ve as one indicator of the classification of H. ducreyi strains.

162 from a geographically diverse collection of H. ducreyi clinical isolates revealed that OmpP2A and Om

163 ts (HFF); Flp1 and Flp2, the determinants of H. ducreyi adherence to HFF cells, were downregulated in

164 rce of heme or iron for the establishment of H. ducreyi infection in humans.

165 stem regulating a proven virulence factor of H. ducreyi.

166 both known and putative virulence factors of H. ducreyi, including the lspB-lspA2 operon, the flp ope

167 Sarkosyl-insoluble cell envelope fraction of H. ducreyi 35000, which indicated that the LspB protein

168 ceae and responded to different fractions of H. ducreyi separated by preparative sodium dodecyl sulfa

169 The cdtA, cdtB, and cdtC genes of H. ducreyi were cloned independently into plasmid vector

170 endent transporters encoded in the genome of H. ducreyi, only the hemoglobin receptor, HgbA, is requi

171 sed to identify a homologue in the genome of H. ducreyi.

172 Recently, a second group of H. ducreyi strains have been identified.

173 Likewise, a single inoculation of H. ducreyi does not protect pigs against subsequent infe

174 To analyze the interaction of H. ducreyi with macrophages, we investigated the ability

175 geographically diverse clinical isolates of H. ducreyi was examined by Western blotting, 5 of the st

176 e was no significant difference in levels of H. ducreyi recovery from mutant- and parent-inoculated b

177 0R was transformed with a plasmid library of H. ducreyi 35000 DNA, and a clone producing the wild-typ

178 we characterized the sap-containing loci of H. ducreyi 35000HP and demonstrated that sapA is express

179 Cell surface lipooligosaccharides (LOS) of H. ducreyi are thought to play important biological role

180 The vast majority of H. ducreyi strains contain high levels of sialic acid (N

181 zed and is representative of the majority of H. ducreyi strains.

182 In this study, we used a swine model of H. ducreyi infection to demonstrate that an experimental

183 roxide and is impaired in the swine model of H. ducreyi infection.

184 An isogenic mutant of H. ducreyi 35000HP with inactivated lspA1 and lspA2 gene

185 We constructed a nonpolar sapA mutant of H. ducreyi 35000HP, designated 35000HPsapA, and compared

186 re we investigate the biosynthetic origin of H. ducreyi sialosides by metabolic incorporation studies

187 and IL10 are associated with the outcome of H. ducreyi infection.

188 Overexpression of H. ducreyi D15 in Escherichia coli resulted in a source

189 gth LOS structures in the pathophysiology of H. ducreyi infection.

190 onal NK cells may facilitate phagocytosis of H. ducreyi.

191 ate that there are two clonal populations of H. ducreyi.

192 eers significantly enhanced proliferation of H. ducreyi-reactive CD4(+) T cells.

193 ndicate that the LspA1 and LspA2 proteins of H. ducreyi are involved, directly or indirectly, in the

194 The recovery rate of H. ducreyi from cultures and the histopathology of biops

195 The recovery rate of H. ducreyi from surface cultures was 16% (n=142) from pa

196 The histopathology and recovery rates of H. ducreyi from surface cultures and biopsies obtained f

197 ibodies (MAbs) to the hemoglobin receptor of H. ducreyi, HgbA.

198 The rates of recovery of H. ducreyi from surface cultures were 8% (n = 130; 95% C

199 )ppGpp and DksA serve as major regulators of H. ducreyi gene expression in stationary phase and have

200 ap transporter plays a role in resistance of H. ducreyi to LL-37.

201 To better understand the role of H. ducreyi CpxRA in controlling virulence determinants,

202 Thus, sialylation of H. ducreyi LOS can be modulated with respect to the stru

203 The genome of the human-passaged strain of H. ducreyi (35000HP) contains two homologous genes whose

204 ted the wild-type and dsrA mutant strains of H. ducreyi in our swine models of chancroid pathogenesis

205 brane protein is conserved in all strains of H. ducreyi tested and is required for the establishment

206 DsrA was expressed by all strains of H. ducreyi tested, except three naturally occurring, avi

207 d noncompetitive and bound to all strains of H. ducreyi tested.

208 test using geographically diverse strains of H. ducreyi, other Haemophilus strains, and other bacteri

209 nal peptide recognized all tested strains of H. ducreyi.

210 odies elicited to nHgbA bound the surface of H. ducreyi and partially blocked hemoglobin binding by n

211 The survival of H. ducreyi in DC may provide a mechanism by which the or

212 spA1 and LspA2 did not inhibit the uptake of H. ducreyi, despite inactivating Src kinases.

213 ontributed significantly to the virulence of H. ducreyi in humans.

214 nd a proton motive force-dependent effect on H. ducreyi's resistance to LL-37 and beta-defensin HBD-3

215 with polyclonal anti-H. ducreyi antiserum or H. ducreyi-specific monoclonal antibodies (MAbs) and flu

216 when PBMCs were incubated with H. ducreyi or H. ducreyi lipooligosaccharide in vitro.

217 Polyclonal H. ducreyi LspB antiserum reacted with a 64-kDa antigen

218 We found that in this population, H. ducreyi, T. pallidum, and herpes simplex virus HSV DN

219 The putative H. ducreyi glycosyltransferase gene (designated lgtA) wa

220 The putative H. ducreyi glycosyltransferase gene was insertionally in

221 c mutants lacking expression of the putative H. ducreyi heptosyltransferase III, the putative glucosy

222 We conclude that T cells that recognize H. ducreyi antigens are recruited to sites experimentall

223 ility shift assays showed that a recombinant H. ducreyi CpxR protein bound the promoter region of the

224 r 4 (TLR4) signaling pathway greatly reduced H. ducreyi-induced IDO production.

225 of the membrane fusion protein MtrC rendered H. ducreyi more sensitive to LL-37 and human beta-defens

226 the mutant proteins in trans in host strain H. ducreyi FX547 hgbA.

227 The wild-type strain H. ducreyi 35000HP readily inhibited phagocytosis, where

228 re enriched in experimental lesions and that H. ducreyi induced IDO transcription in dendritic cells

229 8, 5C9, 3B9, 2C7, and 9D12 demonstrated that H. ducreyi expresses the major pilus subunit, FtpA, the

230 In previous work, we demonstrated that H. ducreyi scavenges sialic acid from the extracellular

231 We also found that H. ducreyi inhibits the phagocytosis of a secondary targ

232 Our study data indicate that H. ducreyi induces NLRP3 inflammasome activation via mul

233 These findings indicate that H. ducreyi-induced IDO expression in DC is largely media

234 tingly, the use of EMSAs also indicated that H. ducreyi CpxR did not bind to the promoter regions of

235 The results of these studies indicated that H. ducreyi requires both the LspA1 and LspA2 proteins to

236 shift assays (EMSAs) were used to prove that H. ducreyi CpxR interacted with the promoter regions of

237 Here we report that H. ducreyi can use unnatural sialic acids bearing elonga

238 adherence in vivo and strongly suggest that H. ducreyi remains extracellular throughout infection an

239 Previous studies suggested that H. ducreyi encounters growth conditions in human lesions

240 While previous reports suggested that H. ducreyi strains formed two clonal populations, the di

241 bacteria were internalized, suggesting that H. ducreyi avoids phagocytosis by human macrophages.

242 terial common antigen (ECA), suggesting that H. ducreyi may express a putative ECA-like glycoconjugat

243 The H. ducreyi lspB gene encodes a protein with a predicted

244 ith two plasmids individually containing the H. ducreyi cdtA and cdtC genes, we purified a noncovalen

245 In contrast, the H. ducreyi lspA1 mutant 35000HP.1, which did not express

246 Here, we determined the H. ducreyi transcriptome in biopsy specimens of human le

247 The gene encoding the H. ducreyi D15 protein was cloned and sequenced, and the

248 several potential regulatory targets for the H. ducreyi CpxRA two-component regulatory system.

249 bvious two-component system contained in the H. ducreyi genome and negatively regulates the lspB-lspA

250 opies of the plasmid are integrated into the H. ducreyi 35000HP genome.

251 Inactivation of the H. ducreyi cpxR gene did not reduce the ability of this

252 Provision of the H. ducreyi luxS gene in trans partially restored AI-2 pr

253 sA compensates for the loss of (p)ppGpp; the H. ducreyi double mutant expressed higher transcript lev

254 receptor, the collagen-binding protein, the H. ducreyi lectin, the fine-tangle pili, and the outer m

255 In the present study, the H. ducreyi CpxR and CpxA proteins were shown to closely

256 Haemophilus influenzae type B, we termed the H. ducreyi protein D15.

257 RT-PCR analysis indicated that the H. ducreyi flp gene cluster was likely to be a polycistr

258 These results indicated that the H. ducreyi LspB protein is involved in secretion of the

259 appeared to be primarily associated with the H. ducreyi cell envelope, whereas both CdtB and CdtC wer

260 The first three open reading frames in this H. ducreyi gene cluster encoded predicted proteins with

261 We have constructed three H. ducreyi 35000HP mutants containing antibiotic resista

262 ed macrophage polarization may contribute to H. ducreyi clearance during human infection.

263 mutant of csrA to assess its contribution to H. ducreyi pathogenesis.

264 e PP and RR groups respond differentially to H. ducreyi.

265 icantly inhibited after a 15-min exposure to H. ducreyi, and a multiplicity of infection of approxima

266 catalyses the alpha2,3 addition of Neu5Ac to H. ducreyi LOS and therefore the terminal side-chain of

267 ts to assess the contribution of (p)ppGpp to H. ducreyi pathogenesis.

268 The lines and clone responded to H. ducreyi antigen in a dose-dependent manner and produc

269 One clone and 12 lines that responded to H. ducreyi antigens were obtained from 12 of the subject

270 ount an effective humoral immune response to H. ducreyi after multiple exposures to the organism.

271 e PP and RR groups shared a core response to H. ducreyi.

272 0 (IL-10) but no IL-4 or IL-5 in response to H. ducreyi.

273 ions suggest that subjects are sensitized to H. ducreyi during the course of infection.

274 were tyrosine phosphorylated after wild-type H. ducreyi cells were incubated with macrophages.

275 s showed that those incubated with wild-type H. ducreyi had greatly reduced phosphorylation levels of

276 This inhibitory effect of wild-type H. ducreyi on phagocytic activity was primarily associat

277 del, 8 of 30 sites inoculated with wild-type H. ducreyi progressed to the pustular stage, compared to

278 Wild-type H. ducreyi strain 35000HP contains two genes, lspA1 and

279 ed that macrophages incubated with wild-type H. ducreyi, but not with a lspA1 lspA2 mutant, were unab

280 but not in HeLa cells, exposed to wild-type H. ducreyi.

281 A mutant (35000HPfgbA) was constructed using H. ducreyi 35000HP, and 6 volunteers were experimentally

282 after the first inoculation contained viable H. ducreyi cells, but this percentage dropped to only 16

283 rst and second inoculations contained viable H. ducreyi cells, yet only 55% of the lesions biopsied 2

284 d viable H. ducreyi cells, whereas no viable H. ducreyi cells were recovered from inoculated sites of

285 ites from mock-immunized pigs yielded viable H. ducreyi cells, whereas no viable H. ducreyi cells wer

286 To study the mechanism by which H. ducreyi activated NK cells, we used peripheral blood

287 This finding suggests a mechanism by which H. ducreyi avoids killing and clearance by macrophages i

288 offered protection against a challenge with H. ducreyi strain 35000HP expressing either class I or c

289 stered to naive pigs prior to challenge with H. ducreyi.

290 ot replicated when PBMCs were incubated with H. ducreyi or H. ducreyi lipooligosaccharide in vitro.

291 DNAs from 105 volunteers infected with H. ducreyi at 3 sites were genotyped for SNPs, using rea

292 d from subjects experimentally infected with H. ducreyi to study the evolution of the immune response

293 n subjects were experimentally infected with H. ducreyi until they developed a painful pustule or for

294 tules obtained from volunteers infected with H. ducreyi were subjected to reverse transcription-PCR.

295 es for 267 volunteers who were infected with H. ducreyi.

296 and cytokines/chemokines upon infection with H. ducreyi in vitro.

297 uld be due either to previous infection with H. ducreyi or to the detection of cross-reacting antibod

298 ng chancroid nor experimental infection with H. ducreyi results in protective immunity.

299 After three successive inoculations with H. ducreyi, pigs developed a modestly protective immune

300 Here, we infected PP and RR subjects with H. ducreyi and used microarrays to profile gene expressi