ライフサイエンスコーパス: Y. pestis

1 Y. pestis biofilm formation has been studied in the rat

2 Y. pestis CU pathways y0348-0352 and y1858-1862 were fou

3 Y. pestis grown at 37 degrees C and pH 7 had equal contr

4 Y. pestis has two well-characterized CU pathways: the ca

5 Y. pestis is capable of causing major epidemics; thus, t

6 Y. pestis lacking Ivy had attenuated virulence, unless a

7 Y. pestis mutants unable to either transport Ybt or synt

8 Y. pestis phoP-negative mutants achieved normal infectio

9 Y. pestis recently evolved from the gastrointestinal pat

10 Y. pestis strains containing deletions in CU pathways y0

11 Y. pestis type III secretion system effectors YopJ and Y

12 A phylogenic tree including 36 Y. pestis strains highlighted an association between the

13 postinfection, a total of 801, 464, and 416 Y. pestis genes were differentially regulated, respectiv

14 a library comprised of approximately 31,500 Y. pestis KIM6+ transposon insertion mutants (input pool

15 nd that plasmid-expressed ExsA complements a Y. pestis lcrF mutant for T3SS gene expression.

16 Recently, a Y. pestis pgm strain was isolated from a researcher with

17 In addition, Y. pestis was identified directly from positive blood cu

18 in the usher genes for six of the additional Y. pestis CU pathways.

19 dependent caspase-1 activation pathway after Y. pestis challenge.

20 trolling IL-18 and IL-1beta production after Y. pestis infection, and NLRP12-deficient mice were more

21 masome activation, and host resistance after Y. pestis infection.

22 arlier work reported that antibodies against Y. pestis LcrV cannot block type III injection by Yersin

23 denced by high serum antibody levels against Y. pestis F1 antigen.

24 onal or monoclonal antibodies raised against Y. pestis KIM D27 LcrV (LcrV(D27)) bind LcrV from Y. ent

25 y play a role in the immune response against Y. pestis in natural hosts.

26 ytokines important to host responses against Y. pestis and many other infectious agents.

27 platform for intranasal vaccination against Y. pestis and other infectious pathogens.

28 proteins based on the roles of their aligned Y. pestis and S. enterica partners and showed that up to

29 All Y. pestis strains, including those phylogenetically clos

30 at Angola belongs to one of the most ancient Y. pestis lineages thus far sequenced.

31 nsus binding sites in both P. aeruginosa and Y. pestis T3SS promoters prevent activation by ExsA and

32 mutants of Y. pseudotuberculosis IP32953 and Y. pestis KIM6+.

33 r known as YopJ in Y. pseudotuberculosis and Y. pestis and YopP in Y. enterocolitica has been shown t

34 conserved between Y. pseudotuberculosis and Y. pestis differs in both timing and dependence on Hfq,

35 suggests that both Y. pseudotuberculosis and Y. pestis produce an oligosaccharide core with a single

36 sceptibility by 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional

37 C P(BAD) crp mutant also developed high anti-Y. pestis and anti-LcrV serum IgG titers but with a more

38 U of the Deltacrp mutant developed high anti-Y. pestis and anti-LcrV serum IgG titers, both with a st

39 progressive stages of the disease with anti-Y. pestis antibodies alone or in combination with the co

40 As Y. pestis further evolved, modern strains acquired a sin

41 ession is an effective strategy to attenuate Y. pestis while retaining strong immunogenicity, leading

42 In contrast, attenuated Y. pestis lacking the conserved pigmentation locus could

43 After vaccinating with live attenuated Y. pestis and challenging intranasally with virulent pla

44 cient mice with D27-pLpxL, a live attenuated Y. pestis strain, induces cell-mediated protection again

45 The development of live, attenuated Y. pestis vaccines may be facilitated by detoxification

46 in the ear with wild-type (WT) or attenuated Y. pestis lacking the pYV virulence plasmid (pYV(-)).

47 DeltamsbB double mutant severely attenuated Y. pestis CO92 to evoke pneumonic plague in a mouse mode

48 -/-) mice with a subunit vaccine that blocks Y. pestis type III secretion generated protection agains

49 nonical drug target for infections caused by Y. pestis and possibly for those caused by other blood-b

50 interaction is important for Yop delivery by Y. pestis.

51 Ail expressed by Y. pestis bound purified fibronectin, as did the Y. pest

52 The rapid killing of macrophages induced by Y. pestis, dependent upon type III secretion system effe

53 fic antibodies blocked type III injection by Y. pestis expressing lcrV(W22703) or lcrV(WA-314) and pr

54 of mice that are cleaved and/or processed by Y. pestis in a Pla-dependent manner.

55 iety on the surface of many mammalian cells, Y. pestis appears to prefer interacting with certain typ

56 of specific plasmid-encoded vs. chromosomal Y. pestis virulence factors in the pathogenesis of acute

57 as shown with recombinant Escherichia coli, Y. pestis, or purified passenger domains.

58 hich could be extremely useful in confirming Y. pestis persistence in the ground.

59 his detrimental effect under proper control, Y. pestis expresses the caf operon (encoding the F1 caps

60 Deletion of ivy decreased Y. pestis' ability to counter lysozyme and polymorphonuc

61 infection with either wild-type or Deltapla Y. pestis, Prdx6-deficient mice exhibit no differences i

62 mpared to that after infection with Deltapla Y. pestis, suggesting that Pla cleaves Prdx6 in the pulm

63 erentially recruited by parent and DeltayopM Y. pestis infections were CCR2(+) Gr1(+) CD11b(+) CD11c(

64 also was shown to be required for DeltayopM Y. pestis to show wild-type growth in skin.

65 When PMNs were ablated from mice, DeltayopM Y. pestis grew as well as the parent strain in liver but

66 red to selectively limit growth of DeltayopM Y. pestis and that CD11b(+) cells other than polymorphon

67 , wild-type growth was restored to DeltayopM Y. pestis in both organs.

68 PhiA1122::luxAB rapidly detects Y. pestis in pure culture and human serum by transducing

69 rom yapJ in its contribution to disseminated Y. pestis infection.

70 eract with YopD within targeted cells during Y. pestis infection, suggesting that YopK's regulatory m

71 contributes to type I IFN expression during Y. pestis infection and suggest that the TLR7-driven typ

72 interferon (IFN) signaling is induced during Y. pestis infection and contributes to neutrophil deplet

73 A fast and efficient Y. pestis dissemination in SEG mice may be critical for

74 inflammatory responses and enables enhanced Y. pestis outgrowth in the lungs.

75 Here, we present six new European Y. pestis genomes spanning the Late Neolithic to the Bro

76 identified has not been found in any extant Y. pestis foci sampled to date, and has its ancestry in

77 Thus, by degrading FasL, Y. pestis manipulates host cell death pathways to facili

78 Here we present five Y. pestis genomes from one of the last European outbreak

79 is not only dispensable but deleterious for Y. pestis virulence.

80 ional regulator YfbA, which is essential for Y. pestis colonization and biofilm formation in cat flea

81 ilable in <4 h for B. anthracis and <6 h for Y. pestis and B. pseudomallei One exception was B. pseud

82 To identify genes that are important for Y. pestis survival in macrophages, a library comprised o

83 rter displayed 100% (n = 59) inclusivity for Y. pestis and consistent intraspecific signal transducti

84 K and PKC inhibitors were selective only for Y. pestis infection.

85 minogen-activating protease (pla) genes from Y. pestis CO92.

86 ies and oxidative stress genes that may help Y. pestis survive at the host temperature.

87 criptional profiling experiments to identify Y. pestis quorum sensing regulated functions.

88 In Y. pestis CO92, the autotransporter genes yapK and yapJ

89 xpression of lcrV(W22703) or lcrV(WA-314) in Y. pestis did not allow these strains to escape LcrV-med

90 severe growth restriction at 37 degrees C in Y. pestis but not in Y. pseudotuberculosis.

91 ructure, blocking effector transport even in Y. pestis yscF variants that are otherwise calcium blind

92 a role for the Yaps as virulence factors in Y. pestis.

93 Deletion mutants of ilp were generated in Y. pestis strains KIM5(pCD1(+)) Pgm(-) (pigmentation neg

94 of yersiniosis, as does the inactivation in Y. pestis of a conserved, Yersinia-specific sRNA in a mo

95 IM6 to identify surface proteins involved in Y. pestis host cell invasion and bacterial virulence.

96 d C9 importer for manganese (Mn) and iron in Y. pestis, might function as a second, high-affinity Zn

97 f the caf operon are minimally manifested in Y. pestis.

98 of rfaH in Y. pseudotuberculosis but not in Y. pestis.

99 We also show that cleavage of YapE occurs in Y. pestis but not in the enteric Yersinia species, and r

100 ting that a noncanonical mechanism occurs in Y. pestis-infected macrophages.

101 The outer membrane protein X (OmpX) in Y. pestis KIM is required for efficient bacterial adhere

102 gene in a strain-specific manner and only in Y. pestis and Y. pseudotuberculosis.

103 ffecting the expression of the feo operon in Y. pestis.

104 er confirmed when they were overexpressed in Y. pestis KIM6+.

105 To assess the genomic plasticity in Y. pestis, we investigated the global gene reservoir and

106 late motility, the role of quorum sensing in Y. pestis has been unclear.

107 ssess the functional role of AI-2 sensing in Y. pestis, microarray studies were conducted by comparin

108 e first global analysis of AI-2 signaling in Y. pestis and identifies potential roles for the system

109 Studies in Y. pestis and Y. pseudotuberculosis have shown that YopM

110 y apparent high-affinity Zn uptake system in Y. pestis.

111 he unidentified, secondary Zn transporter in Y. pestis.

112 hatase, LpxE, from Francisella tularensis in Y. pestis yields predominantly 1-dephosphorylated lipid

113 m a variety of pathogenic bacteria including Y. pestis, H. influenzae, and Proteus that cause plague,

114 potential agents of bioterrorism, including Y. pestis.

115 lence in many bacterial pathogens, including Y. pestis, any change in autotransporter content should

116 Pathogenic Yersinia, including Y. pestis, the agent of plague in humans, and Y. pseudot

117 were significantly induced in intracellular Y. pestis, consistent with the presence of oxidative str

118 n insights into the biology of intracellular Y. pestis and its environment following phagocytosis, we

119 erived from the recognition of intracellular Y. pestis by host Toll-like receptor 7 (TLR7).

120 the same intradermal site with purified LPS, Y. pestis did not prevent recruitment of neutrophils.

121 of a functional ureD was sufficient to make Y. pestis orally toxic to fleas.

122 inst pneumonic plague challenge with 250 MLD Y. pestis CO92, immunization with recombinant F1 did not

123 genetic make-up intermediate between modern Y. pestis isolates and its evolutionary ancestor, Y. pse

124 pathogenic potential is distinct from modern Y. pestis isolates.

125 R10 single-nucleotide polymorphisms modulate Y. pestis-induced cytokine responses.

126 The YPTB3286-like gene of most Y. pestis strains appears to be inactivated, perhaps in

127 m, but not mouse serum, to kill ail-negative Y. pestis in vitro.

128 -/-) mice were not protected by neutralizing Y. pestis antibodies, yet bacterial growth in the lungs

129 stores the virulence defects of nonpigmented Y. pestis.

130 o include homologous sequences from numerous Y. pestis and Y. pseudotuberculosis strains, we determin

131 s studies have indicated that the ability of Y. pestis to survive inside macrophages may be critical

132 stic basis of the evolutionary adaptation of Y. pestis to flea-borne transmission.

133 These findings reveal adaptations of Y. pestis to the dermis and how these adaptations can de

134 ains, suggesting an evolutionary adaption of Y. pestis to specific local animal hosts or reservoirs.

135 delivery, we deleted five known adhesins of Y. pestis.

136 ion of 1- and 12-microm-particle aerosols of Y. pestis in the lower and upper respiratory tracts (URT

137 may contribute to the severe attenuation of Y. pestis lacking this RNA chaperone in animal models of

138 ian lethal doses (LD50) (2.4 x 10(4) CFU) of Y. pestis KIM6+(pCD1Ap) than chi10057(pYA3332) (40% surv

139 ed infection kinetics and early clearance of Y. pestis.

140 Here, we demonstrate that omptin cleavage of Y. pestis YapE is required to mediate bacterial aggregat

141 ucosamine to the lipooligosaccharide core of Y. pestis.

142 mice were infected with equal CFU counts of Y. pestis.

143 We conclude that, throughout the course of Y. pestis infection, OmpR-EnvZ is required to counter to

144 binding and delivery of Yops (cytotoxins of Y. pestis), a novel interaction, distinct from other bac

145 ver, we report the first direct detection of Y. pestis in soil, which could be extremely useful in co

146 lture), sensitive, and specific detection of Y. pestis in such complex samples.

147 tightly controlled virulence determinant of Y. pestis.

148 y adaptation that followed the divergence of Y. pestis from the closely related food- and waterborne

149 cquisition of pPCP1 during the divergence of Y. pestis from Y. pseudotuberculosis, and are the first

150 tant steps in the evolution and emergence of Y. pestis as a flea-borne pathogen.

151 The emergence of Y. pestis fits evolutionary theories that emphasize ecol

152 ts show that a key event in the evolution of Y. pestis from the ancestral Yersinia pseudotuberculosis

153 ors, ureD mutation early in the evolution of Y. pestis was likely subject to strong positive selectio

154 dentified Ilp as a novel virulence factor of Y. pestis.

155 Thus, an important feature of Y. pestis infection is reduced activation and organizati

156 ed that the highly conserved Psa fimbriae of Y. pestis (also called pH 6 antigen) are expressed in mu

157 age formation and acquisition and fitness of Y. pestis during flea gut infection, consistent with pos

158 secretion, a critical virulence function of Y. pestis.

159 Thus, the interactions of Y. pestis with its flea vector that lead to colonization

160 ers of IgG response to whole-cell lysates of Y. pestis (YpL) and subunit LcrV similar to those seen w

161 Using established mouse models of Y. pestis infection, we demonstrated that despite the hi

162 esults indicate that the smpB-ssrA mutant of Y. pestis possesses the desired qualities for a live att

163 these observations, the smpB-ssrA mutant of Y. pestis was severely attenuated in a mouse model of in

164 agenic approach, we created 5,088 mutants of Y. pestis strain CO92 and screened them in a mouse model

165 P-PhoQ system, OmpR-EnvZ was the only one of Y. pestis' 23 other 2CSs required for production of bubo

166 ole for pneumonic plague during outbreaks of Y. pestis infections.

167 ifies three of the additional CU pathways of Y. pestis as mediating interactions with host cells that

168 Although an initial intracellular phase of Y. pestis infection has been postulated, a Th1-type cyto

169 e lcrV gene on the pCD1 virulence plasmid of Y. pestis KIM D27 with either lcrV(W22703) or lcrV(WA-31

170 gative selection screen using a vast pool of Y. pestis mutants revealed no selection against any know

171 d the genome-wide transcriptional profile of Y. pestis KIM5 replicating inside J774.1 macrophage-like

172 culosis, the relatively recent progenitor of Y. pestis, shows no similar trans-complementation effect

173 r capacity to modulate binding properties of Y. pestis in its hosts, in conjunction with other adhesi

174 participate in broadening the host range of Y. pestis.

175 mpounded fears of the intentional release of Y. pestis as a biological weapon.

176 resolve conflicting evidence for the role of Y. pestis lipopolysaccharide (LPS) and OmpX in serum res

177 The discovery of molecular signatures of Y. pestis in prehistoric Eurasian individuals and two ge

178 The formation of fibrin at sites of Y. pestis infection supports innate host defense against

179 a possible scenario for the early spread of Y. pestis: the pathogen may have entered Europe from Cen

180 of mice with the smpB-ssrA mutant strain of Y. pestis induced a strong antibody response.

181 ks in detecting capsular-positive strains of Y. pestis in bubonic and pneumonic plague.

182 the most ancestral, deeply rooted strains of Y. pestis to cause pneumonic plague, indicating that Y.

183 genes known to be important for survival of Y. pestis in macrophages, including phoPQ and members of

184 wecB and wecC), is important for survival of Y. pestis in macrophages.

185 ntiport is indispensable for the survival of Y. pestis in the bloodstreams of infected animals and th

186 le immune environment leading to survival of Y. pestis within the eukaryotic host.

187 00-fold and 10,000-fold higher than those of Y. pestis KIM5+, respectively, indicating that both stra

188 ly infected with 109 colony-forming units of Y. pestis attenuated strains CO99 (pCD1+/DeltaApgm) or K

189 accharide function, reduced the virulence of Y. pestis CO92 in mouse models of bubonic and pneumonic

190 tion alone had no effect on the virulence of Y. pestis in either bubonic or pneumonic plague models.

191 ded no significant reduction in virulence of Y. pestis in mice when it was administered i.n. but actu

192 e background indicates that the virulence of Y. pestis is dependent on the genetic makeup of its host

193 of LpxE does not attenuate the virulence of Y. pestis.

194 factor in evolution of the high virulence of Y. pestis.

195 Of these five strains, only Y. pestis DeltaphoPQ demonstrated global sensitivity to

196 through tight regulation of the caf operon, Y. pestis precisely balances its capsular anti-phagocyti

197 R2 agonist), E. coli LPS (a TLR4 agonist) or Y. pestis infection, while the PI3K and PKC inhibitors w

198 DeltayopM mutant was relieved by the parent Y. pestis strain in a coinfection assay in which the par

199 ctively lost in spleens infected with parent Y. pestis.

200 Unlike other bacterial pathogens, Y. pestis does not require Znu for high-level infectivit

201 osis; however, it is not known at what point Y. pestis gained the ability to induce a fulminant pneum

202 od vector prior to transmission may preadapt Y. pestis to resist the initial encounter with the mamma

203 Two prime Y. pestis vaccine candidates are the usher-chaperone fim

204 17-kDa outer membrane protein that protects Y. pestis against complement-mediated lysis, on bubonic

205 e that enhances protection against pulmonary Y. pestis challenge, and we suggest that pneumonic plagu

206 mediated protection against lethal pulmonary Y. pestis challenge.

207 receptor CXC receptor 2 (CXCR2) to pulmonary Y. pestis infection.

208 ent with its lack of coordination to purine, Y. pestis AC-IV cyclizes both ATP and GTP.

209 in vivo; the role of A2AP during respiratory Y. pestis infection is not known either.

210 edundant roles for yapJ and yapK in systemic Y. pestis infection.

211 in response to Y. pestis infection, and that Y. pestis entry into macrophages may involve the partici

212 Thus, we conclude that Y. pestis YopJ and YopM can both exert a tight control o

213 These findings demonstrate that Y. pestis Ail uses multiple extracellular loops to inter

214 Importantly, we find that Y. pestis containing combined deletions of YopJ and YopM

215 in Yersinia pestis virulence and found that Y. pestis strains lacking the major Na(+)/H(+) antiporte

216 These findings indicate that Y. pestis was capable of causing pneumonic plague before

217 s to cause pneumonic plague, indicating that Y. pestis was primed to infect the lungs at a very early

218 We propose that Y. pestis utilizes Hfq to link c-di-GMP levels to enviro

219 Herein we report that Y. pestis requires, in a nonredundant manner, both PsaA

220 In this study, we report that Y. pestis YopE is a dominant Ag recognized by CD8 T cell

221 Here, we show that Y. pestis does not appreciably cleave A2AP in a Pla-depe

222 Here, we show that Y. pestis infects and replicates as a biofilm in the for

223 o genomes from Southern Siberia suggest that Y. pestis caused some form of disease in humans prior to

224 The Y. pestis adhesin Ail facilitates Yop translocation and

225 The Y. pestis adhesin Ail mediates host cell binding and is

226 The Y. pestis ail mutant was attenuated for virulence in bot

227 The Y. pestis Ail protein is an important bubonic plague vir

228 The Y. pestis derivative strain lacking the nhaA and nhaB ge

229 The Y. pestis genome contains additional CU pathways that ar

230 The Y. pestis KIM5 Deltailp strain had reduced adhesion to a

231 The Y. pestis outer membrane Pla protease is essential for t

232 hree relevant protein markers encoded by the Y. pestis-specific plasmids pFra (murine toxin) and pPla

233 Under static growth conditions, the Y. pestis feo::lacZ fusion was repressed by iron in a Fu

234 estis bound purified fibronectin, as did the Y. pestis adhesin plasminogen activator (Pla).

235 ate that omptin cleavage is specific for the Y. pestis and Y. pseudotuberculosis YapE orthologues but

236 deliver high-level protection; however, the Y. pestis Ags recognized by cytokine-producing T cells h

237 orm a single putatively extinct clade in the Y. pestis phylogeny.

238 Expression of the Y. pestis F1 capsule was not required for the developmen

239 o significant effect on transcription of the Y. pestis feo promoter.

240 r nhaB in trans restored the survival of the Y. pestis nhaA nhaB double deletion mutant in blood.

241 ocking infection depends on induction of the Y. pestis PhoP-PhoQ two-component regulatory system in t

242 Through deep sequencing analysis of the Y. pestis sRNA-ome, we found 63 previously unidentified

243 ppears to be a major in vivo function of the Y. pestis virulence plasmid.

244 We examined binding of the Y. pestis WT and usher deletion strains to A549 human lu

245 This study focuses on the Y. pestis KIM yapV gene and its product, recognized as a

246 activator protease), which is encoded on the Y. pestis-specific plasmid pPCP1.

247 -dependent addition of aminoarabinose to the Y. pestis lipid A, because an aminoarabinose-deficient m

248 Thus, Y. pestis-orchestrated LN remodeling promoted its dissem

249 One mechanism contributing to Y. pestis virulence is the presence of a type-three secr

250 1 day prior to lethal pulmonary exposure to Y. pestis strain KIM D27 significantly improves survival

251 arify the contributions of these proteins to Y. pestis pathogenesis.

252 ytokine response, and a higher resistance to Y. pestis-induced apoptosis.

253 kinetics and extent of the host response to Y. pestis and how it is influenced by the Yersinia virul

254 ulus for NF-kappaB activation in response to Y. pestis infection, and that Y. pestis entry into macro

255 This response was not specific to Y. pestis and involved a reduced sensitivity to M2 polar

256 dification of YapE appears to be specific to Y. pestis, was acquired along with the acquisition of pP

257 signaling led to increased susceptibility to Y. pestis, producing tetra-acylated lipid A, and an atte

258 RNA interference enhances susceptibility to Y. pestis.

259 nd that B10.T(6R) mice become susceptible to Y. pestis infection by the age of 5 months.

260 pseudotuberculosis, while yapJ is unique to Y. pestis.

261 r testing antimicrobial agents used to treat Y. pestis, except for chloramphenicol and trimethoprim-s

262 issemination and multiplication of wild-type Y. pestis during the bubonic stage of disease did not in

263 Additionally, LpxE synthesis in wild-type Y. pestis KIM6+(pCD1Ap) led to slight attenuation by s.c

264 tion, we found that infection with wild-type Y. pestis reduces the abundance of extracellular Prdx6 i

265 rly, lungs of mice challenged with wild-type Y. pestis show reduced levels of FasL and activated casp

266 Wild-type Y. pestis, but not a Pla mutant (Deltapla), degrades Fas

267 ing bacterial spread is key to understanding Y. pestis and the immune responses it encounters during

268 chanisms that are effective against virulent Y. pestis, raising new insight into the activation of ne

269 to disease progression in the fully virulent Y. pestis CO92 strain by engineering a deletion mutant a

270 ubcutaneously infected with a fully virulent Y. pestis strain and treated at progressive stages of th

271 ltamsbB double mutant of the highly virulent Y. pestis CO92 strain.

272 o quantitate the internalization of virulent Y. pestis CO92 by macrophages and the subsequent activat

273 ter subcutaneous infection with the virulent Y. pestis CO92.

274 against subcutaneous challenge with virulent Y. pestis (80% survival) but no protection against pulmo

275 t lethal intranasal challenges with virulent Y. pestis.

276 In vivo, Y. pestis lacking OmpR-EnvZ did not induce an early immu

277 icity to the flea vectors of plague, whereas Y. pestis does not.

278 However, the mechanism by which Y. pestis promotes its intracellular survival is not wel

279 late (c-di-GMP), but the mechanisms by which Y. pestis regulates c-di-GMP synthesis and turnover are

280 et al. (2014) explore the mechanism by which Y. pestis spreads and thus leads to this striking lympha

281 d-and water-borne enteric species from which Y. pestis diverged less than 6,400 y ago, exhibits signi

282 e of Yersinia pseudotuberculosis, from which Y. pestis diverged only within the last 20000 years.

283 gest a step-wise evolutionary model in which Y. pestis emerged as a flea-borne clone, with each genet

284 ost recent 19(th) century pandemic, in which Y. pestis spread worldwide [5] and became endemic in sev

285 Following intravenous challenge with Y. pestis KIM5 Deltailp, mice had a delayed time to deat

286 otection against subcutaneous challenge with Y. pestis strain CO92 even though it fails to protect mi

287 protected mice against lethal challenge with Y. pestis strain CO92 introduced through either the intr

288 tive against lethal pulmonary challenge with Y. pestis.

289 sistant to lethal intravenous challenge with Y. pestis.

290 developed lethal plague when challenged with Y. pestis pgm strains.

291 uitment to the lungs of mice challenged with Y. pestis, this impact is equally evident in mice that r

292 e with host sensing of YscF, consistent with Y. pestis pathogenesis.

293 ysis on Caenorhabditis elegans infected with Y. pestis shows enrichment in genes that are markers of

294 hermore, following intranasal infection with Y. pestis, A2AP-deficient mice exhibit no difference in

295 apoptotic death pathway after infection with Y. pestis, influenced by Toll-like receptor 4-TIR-domain

296 F1-specific antibodies interfere with Y. pestis type III transport of effector proteins into h

297 defense in mice challenged intranasally with Y. pestis.

298 Intranasal challenge in mice with Y. pestis CO92 Deltailp had a 55-fold increase in the 50

299 we found that the genomic plasticity within Y. pestis clearly was not as limited as previously thoug

300 which require help from fibrin to withstand Y. pestis encounters and effectively clear bacteria.