ライフサイエンスコーパス: B. anthracis

1 B. anthracis and other pathogenic B. cereus isolates har

2 B. anthracis carries two copies of the ccdA gene, encodi

3 B. anthracis causes natural infection in humans and anim

4 B. anthracis does not elaborate wall teichoic acids; how

5 B. anthracis does not synthesize these polymers, yet its

6 B. anthracis gneY (BAS5048) and gneZ (BAS5117) encode ne

7 B. anthracis growth was locally controlled for 6 hours.

8 B. anthracis infection also induced a similar enteric ba

9 B. anthracis mutants lacking ltaS1, ltaS2, ltaS3, or lta

10 B. anthracis PGA persisted longer in high m.w. form in m

11 B. anthracis secretes two NEAT hemophores, IsdX1 and Isd

12 B. anthracis strains were monitored over time in the pre

13 B. anthracis vesicles formed at the outer layer of the b

14 RS and well below the infective dose of 10(4)B. anthracis cells for inhalation anthrax.

15 A B. anthracis strain lacking the HtrC protease did not ge

16 In the presence of excess CapD, a B. anthracis gamma-glutamyl transpeptidase, the protecti

17 We created a B. anthracis mutant strain altered in lipoproteins by de

18 le of atxA in virulence factor expression, a B. anthracis atxA-null mutant is avirulent in a murine m

19 InhA1 purified from a B. anthracis culture supernatant directly cleaved each o

20 The virulence of a B. anthracis strain from which the ccpA gene was deleted

21 We demonstrated that a B. anthracis DeltaexsB mutant unable to synthesize ExsB

22 Here, we present evidence that a B. anthracis S-layer homology (SLH) protein harboring a

23 anthracis protective Ag (PA) together with a B. anthracis edema factor (EF) mutant having reduced ade

24 ved significantly longer than controls after B. anthracis challenge.

25 bacterial activity by human NK cells against B. anthracis bacilli within infected autologous monocyte

26 he mechanism by which MyD88 protects against B. anthracis infection, knockout mice were challenged wi

27 cipate in the innate immune response against B. anthracis and suggest that immune modulation to augme

28 thracis Ames ancestor, the progenitor of all B. anthracis Ames strains.

29 omplexity of germination responses may allow B. anthracis spores to respond to different environments

30 Although B. anthracis has undergone an ecological shift within th

31 ore efficient at internalizing S. aureus and B. anthracis compared with E. coli Alveolar macrophages

32 I = CC(50)/MIC) values against S. aureus and B. anthracis for compound 20 were 33 and 66 and for comp

33 iensis that sets it apart from B. cereus and B. anthracis is the production of crystal (Cry) proteins

34 e associated with virulence in B. cereus and B. anthracis, respectively.

35 n virulence regulation between B. cereus and B. anthracis.

36 sequencer (MinION) for Y. pestis (6.5 h) and B. anthracis (8.5 h) and sequenced strains with differen

37 s upon the uptake of both microparticles and B. anthracis Sterne 34F2 spores.

38 thracis DNA into individual PCR mixtures and B. anthracis CFU into human blood.

39 treptogramin resistance protein, MLSRP), and B. anthracis (sul1), respectively.

40 acillus anthracis, Bordetella pertussis, and B. anthracis (sulfonamide resistance gene, sul1), respec

41 sis subspecies tularensis strain SCHU S4 and B. anthracis Ames.

42 cular link between environmental sensing and B. anthracis pathogenesis.

43 We show that lethal toxin and B. anthracis challenge induce bacteremia as a result of

44 rofiles of each of the two F. tularensis and B. anthracis strains exhibited some similarities.

45 F. tularensis and B. anthracis were grown in liquid broth for time periods

46 subspecies novicida and Bacillus anthracis (B. anthracis) Sterne, surrogates for potential bacterial

47 Ps@BNNSs) and conjugated with the mouse anti-B. anthracis Sap antibodies (Ab2); named Au-Pd NPs@BNNSs

48 As B. anthracis is not known to be motile, to be naturally

49 ely detect biological warfare agents such as B. anthracis, emergency responders can implement protoco

50 fficient to render the strain as virulent as B. anthracis Ames.

51 Liquid culture studies with S. aureus , B. anthracis , E. coli , and several other bacterial pat

52 Thus, similar to S. aureus, B. anthracis employs LtaS enzymes to synthesize LTA, an

53 Like several medically important bacteria, B. anthracis lacks glutathione but encodes many genes an

54 antly, in contrast to Sterne, the BaDeltaSET B. anthracis is avirulent in a lethal murine bacteremia

55 moving the focus toward interactions between B. anthracis and lymphoid and epithelial tissues.

56 o investigate the early interactions between B. anthracis spores and cutaneous tissue, spores were in

57 d by interorganizational coauthorships, both B. anthracis and Ebola virus research networks expanded

58 ished that the collagen-like regions of both B. anthracis and B. cereus are similarly substituted by

59 A duplex strand-unwinding activities of both B. anthracis and S. aureus helicases without affecting t

60 targets to halt deadly infections caused by B. anthracis and other pathogenic bacteria and suggest n

61 result in lethal infection of C. elegans by B. anthracis.

62 The exotoxins secreted by B. anthracis use capillary morphogenesis protein 2 (CMG2

63 lved in inflammation, as being suppressed by B. anthracis.

64 Using an experimental model of s.c. B. anthracis infection (an encapsulated nontoxigenic str

65 an and plant pathogens, including B. cereus, B. anthracis, and B. thuringiensis.

66 in the B. cereus group, including B. cereus, B. anthracis, and B. thuringiensis.

67 idase function that is apparent in B. cereus/B. anthracis.

68 e to death (TTD) of wild type and complement B. anthracis Sterne in the A/J mouse model.

69 In contrast, B. anthracis strains lacking both ltaS1 and ltaS2 were u

70 (LT) and edema toxin (ET) could contribute, B. anthracis cell wall peptidoglycan (PGN), not the toxi

71 itant administration of alpha-GalCer delayed B. anthracis systemic dissemination and prolonged mouse

72 eloped a rapid and sensitive assay to detect B. anthracis bacteremia using a system that is suitable

73 DIC during B. anthracis infection may be related more to components

74 r disruption and vascular dysfunction during B. anthracis infection.

75 shed from an active culture of encapsulated B. anthracis strain Ames in blood.

76 capsule derived from wild-type encapsulated B. anthracis Ames (WT) or a control preparation from an

77 owth of both the fully virulent encapsulated B. anthracis Ames and the non-encapsulated Sterne strain

78 s by acting as a "heme sponge" that enhances B. anthracis replication in iron-starved environments.

79 re identified in single-colony environmental B. anthracis Ames isolates associated with the investiga

80 netic parameters and binding order for every B. anthracis spore germinant pair.

81 vity against intracellular and extracellular B. anthracis.

82 For B. anthracis and most other infectious diseases, knowled

83 timicrobial susceptibility by 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to

84 array protein (Sap), a unique biomarker for B. anthracis can offer an opportunity for specific detec

85 The tagO gene appears essential for B. anthracis growth and complements the tagO mutant phen

86 Results were available in <4 h for B. anthracis and <6 h for Y. pestis and B. pseudomallei

87 The detection limit for B. anthracis was found to be 50,000 endospores, on the b

88 8.5 CFU/ml for F. tularensis, 10 CFU/ml for B. anthracis, and 4.5 CFU/ml for Y. pestis The sensitivi

89 were markedly higher than those reported for B. anthracis Ames and more like those of the toxigenic b

90 how that gneZ, but not gneY, is required for B. anthracis vegetative growth, rod cell shape, S-layer

91 stem as a new mutational analysis system for B. anthracis.

92 rapid antimicrobial susceptibility test for B. anthracis This method is based on automated digital t

93 ter-based detection cartridge and tested for B. anthracis on a GeneXpert instrument.

94 t requires a 16- to 20-h incubation time for B. anthracis Advances in high-resolution optical screeni

95 ublished 50% lethal dose (LD(50)) values for B. anthracis Ames after aerosol inoculation.

96 e of AtxA1 is identical to that of AtxA from B. anthracis, while the sequences of AtxA1 and AtxA2 are

97 In this work, cAMP from B. anthracis edema toxin (ET) is found to activate the N

98 n, enhancer-of-zeste, trithorax protein from B. anthracis (BaSET) methylates human histone H1, result

99 type Ib ribonucleotide reductase (RNR) from B. anthracis in the presence of NADPH and thioredoxin re

100 The purification of soluble SlaP from B. anthracis-cleared lysates did not reveal a specific l

101 ns to exploit host innate defenses to hinder B. anthracis colonization.

102 To further understand and compare how B. anthracis disseminates from these two different envir

103 ed to provide a comprehensive picture of how B. anthracis alters host physiology.

104 To understand how B. anthracis acquires iron from heme sources, which acco

105 r point-of-care detection rapidly identifies B. anthracis directly from blood with high sensitivity.

106 To determine if B. anthracis PGA confers a pathogenic advantage over oth

107 In B. anthracis and Bacillus subtilis htrC mutants, YpeB wa

108 In B. anthracis, S-layer proteins and BSLs attach via their

109 is-->Ala) amino acid changes for activity in B. anthracis cultures and for protein-protein interactio

110 Expression of ltaS1 or ltaS2 alone in B. anthracis as well as in other microbes was sufficient

111 Thus, lipoprotein biosynthesis in B. anthracis is required for full virulence in a murine

112 icate that ccdA2 encodes the primary CcdA in B. anthracis, active in all three pathways.

113 ate the roles of the two ccdA gene copies in B. anthracis, strains were constructed without each ccdA

114 for the restriction of m6A-containing DNA in B. anthracis remain unidentified, and we suggest that po

115 ficient replication of hemimethylated DNA in B. anthracis.

116 tudy provides the first evidence of DSPKs in B. anthracis that belong to different classes and have d

117 n the question of what additional factors in B. anthracis are responsible for iron uptake from the mo

118 at cwlT was needed for ICEBs1 to function in B. anthracis.

119 identify a novel role for the yceGH genes in B. anthracis Sterne virulence and suggest that C. elegan

120 tes the relationship between SleB, a GSLE in B. anthracis, and YpeB, a protein necessary for SleB sta

121 siology and pathogenesis was investigated in B. anthracis Sterne.

122 evidence of recent large-scale gene loss in B. anthracis or for unusual accumulation of nonsynonymou

123 o GBAA_pXO1_0023 is not stably maintained in B. anthracis, whereas the full-size parent pXO1 plasmid

124 etic tools developed for DNA manipulation in B. anthracis (Cre-loxP and Flp-FRT systems) were used to

125 r translocation to enhance H1 methylation in B. anthracis-infected macrophages.

126 equences of convergent anthrose mutations in B. anthracis.

127 These genotypes were identified only in B. anthracis morphotypes isolated from the letters, indi

128 e directly linked to sporulation pathways in B. anthracis and more specifically to the regulation of

129 ns required for the import of petrobactin in B. anthracis.

130 ed by GBAA5330 and GBAA4766 respectively) in B. anthracis iron acquisition and pathogenesis.

131 Our results indicate that toxin secretion in B. anthracis is, at least, partially vesicle-associated,

132 sporulation genes spo0A, spo0B, and spo0F in B. anthracis Sterne resulted in phage resistance with co

133 ortant general disulfide reductase system in B. anthracis is TR1/Trx1 and that Trx1 is the physiologi

134 sm of protein attachment to the cell wall in B. anthracis we investigated the structure, backbone dyn

135 , several Gram-positive pathogens, including B. anthracis, contain genes that encode near iron transp

136 illus and Bacillus-related species including B. anthracis.

137 igate many other Bacillus species, including B. anthracis and even "non-pathogenic" Bacillus subtilis

138 Murine inhalational B. anthracis infections have two portals of entry, the n

139 T) or a control preparation from an isogenic B. anthracis Ames strain that produces only 2% of the ca

140 However, like B. anthracis, full virulence of B. cereus G9241 for mice

141 mL with a minimum detection limit of 1 pg/mL B. anthracis Sap antigen.

142 sublethal anthrax infections, encounter most B. anthracis in the wet season and can partially booster

143 ening of a library of transposon-mutagenized B. anthracis spores identified a mutant displaying an al

144 We also used mutant B. anthracis strains to determine the effects on BclA gl

145 ples drawn from patients with concurrent non-B. anthracis bacteremia or nonbacteremic controls.

146 Assay specificity was 100% for tests of non-B. anthracis bacterial isolates and patient blood sample

147 e those of the toxigenic but nonencapsulated B. anthracis Sterne.

148 The ability of B. anthracis to cause anthrax is attributed to the plasm

149 ce of toxin did not influence the ability of B. anthracis to traffic to draining lymph nodes, but sys

150 contrast to other bacteria, O-acetylation of B. anthracis peptidoglycan is combined with N-deacetylat

151 iple inputs and may reflect an adaptation of B. anthracis to changing iron reservoirs during an infec

152 Using kinetic analysis of B. anthracis spores germinated with inosine and L-alanin

153 sed at the same time in sporulating cells of B. anthracis and immediately colocalize to high-molecula

154 unological pathway leading to the control of B. anthracis infection, a finding that might lead to imp

155 No report is available for the detection of B. anthracis by using atxA an anthrax toxin activator ge

156 fer an opportunity for specific detection of B. anthracis in culture broth.

157 developed a rapid protocol for detection of B. anthracis on clinical swabs.

158 immunosensor for ultrasensitive detection of B. anthracis Sap antigen.

159 ptamer sensor for a single-step detection of B. anthracis spore simulant (B. cereus spore).

160 t was found to provide enhanced detection of B. anthracis Sterne strain (34F2) spores relative to the

161 netic approach to search for determinants of B. anthracis chain length, we identified mutants with in

162 r developing species-specific diagnostics of B. anthracis spores and thus targeted therapeutic interv

163 the host environment alter dissemination of B. anthracis depending on the site of initial colonizati

164 produce a map of the global distribution of B. anthracis as a proxy for anthrax risk.

165 at BslO effects a non-random distribution of B. anthracis chain lengths, implying that all septa are

166 ons, by evaluating the terminal diversity of B. anthracis in anthrax carcasses.

167 crucial landmark dictating the emergence of B. anthracis, the evolution of this species and its clos

168 Protein assembly in the envelope of B. anthracis requires S-layer homology domains (SLH) wit

169 s were used to detect LTA in the envelope of B. anthracis strain Sterne (pXO1(+) pXO2(-)) vegetative

170 the genetic background for the evolution of B. anthracis virulence, we obtained high-redundancy geno

171 The geographic extent of B. anthracis is poorly understood, despite multi-decade

172 In extracts of B. anthracis, Trx1 was responsible for almost all of the

173 Among the virulence factors of B. anthracis is the S-layer-associated protein BslA, whi

174 th very high similarities to the sap gene of B. anthracis.

175 to vegetative growth, neither germination of B. anthracis spores nor the formation of spores in mothe

176 ents that stimulate premature germination of B. anthracis spores, greatly simplifying decontamination

177 es of PrkD and PrkG and affect the growth of B. anthracis cells, indicating a possible role of these

178 om BaPGN-treated cells altered the growth of B. anthracis Sterne, and this effect was blocked by LT,

179 itable tools for the rapid identification of B. anthracis.

180 hat culture is not reliable for isolation of B. anthracis from swabs at >/= 7 days.

181 patA1 and patA2 affect the chain lengths of B. anthracis vegetative forms and perturb the deposition

182 The majority of B. anthracis spores in the lung were tightly associated

183 hrax meningitis is a common manifestation of B. anthracis infection, has high mortality, and requires

184 aring model predictions with measurements of B. anthracis spores made after one of the 2001 anthrax l

185 Here we propose a new "jailbreak" model of B. anthracis dissemination which applies to the dissemin

186 ens, elicits protection in a murine model of B. anthracis infection.

187 n inhalational and cutaneous mouse models of B. anthracis infection.

188 ding site, and in vivo, surface molecules of B. anthracis spores promoted GALT development.

189 An FtsX mutant of B. anthracis known to be resistant to the antimicrobial

190 ed approximately 5,000 transposon mutants of B. anthracis Sterne for decreased virulence.

191 s within the anthrose biosynthetic operon of B. anthracis strains from Chile and Poland.

192 ine IL-15 and the protective antigen (PA) of B. anthracis into the Wyeth vaccinia virus.

193 y modifying the general secretory pathway of B. anthracis to transport large amounts of Sap and EA1.

194 have previously shown that peptidoglycan of B. anthracis can induce the production of proinflammator

195 We conclude that peptidoglycan of B. anthracis is initially bound by an unknown extracellu

196 report a novel mechanism for phagocytosis of B. anthracis spores.

197 e modeling, to intrainfection populations of B. anthracis to derive estimates for the duration of the

198 sicle preparations confirmed the presence of B. anthracis toxin components.

199 s anthracis NrdF and the redox properties of B. anthracis NrdI.

200 etA (Bacillus exosporium-targeted protein of B. anthracis).

201 p and EA1 (Eag), the two S-layer proteins of B. anthracis, but not for the secretion of S-layer-assoc

202 of over half of all the secreted proteins of B. anthracis.

203 model parameters (e.g., release quantity of B. anthracis spores, risk of illness, spore setting velo

204 ed that the SETS yielded greater recovery of B. anthracis from 1-day-old swabs; however, reduced viab

205 The collagen-like region of B. anthracis is known to be densely substituted by unusu

206 plays a prominent role in the replication of B. anthracis in hematogenous environments.

207 pid, extensive, and efficient replication of B. anthracis in host tissues makes this pathogen an exce

208 ils in the dLNs, leading to the restraint of B. anthracis dissemination.

209 We investigated the roles of B. anthracis capsule and toxins in the pathogenesis of i

210 re, we report the detection of a simulant of B. anthracis (B. globigii) alone and in a mixture with a

211 globigii (Bg), which serves as a simulant of B. anthracis (or anthrax) and which possesses a peptidog

212 ment for a label-free measurement on site of B. anthracis spore simulant.

213 -LD(50) challenge with aerosolized spores of B. anthracis Ames strain.

214 Moreover, spores of B. anthracis were significantly better at persisting in

215 XO2-61 (or pXO1-118) inhibits sporulation of B. anthracis in a BA2291-dependent manner, and pXO2-61 e

216 This strain of B. anthracis can potentially serve as a preferred host f

217 A mutant strain of B. anthracis deficient in the BshA glycosyltransferase f

218 s hypothesis, we engineered three strains of B. anthracis Sterne, each marked with a different fluore

219 s in growth characteristics among strains of B. anthracis, which is considered to be a clonal organis

220 Ebola virus but contracted for the subset of B. anthracis research that did not involve possession of

221 tripped the PDGA capsule from the surface of B. anthracis Pasteur within 5 min.

222 tic pathway is required for the virulence of B. anthracis in guinea pigs.

223 Reducing the m.w. of B. anthracis PGA reduced monocytes' cytokine responses.

224 The mature cell wall of B. anthracis is resistant to digestion by CwlT, indicati

225 uctural role in stabilizing the cell wall of B. anthracis.

226 alone exhibited little sporicidal effect on B. anthracis spores, while treatment with H(2)O(2) or Na

227 e likely to have significant implications on B. anthracis pathogenesis and microbial manipulation of

228 imicrobial chemicals, H(2)O(2) and NaOCl, on B. anthracis spores.

229 sion of host transcription as well as proper B. anthracis growth, making it a potentially unique viru

230 The loss of both HmoA and IsdG renders B. anthracis incapable of causing anthrax disease.

231 e end, all 27 test set samples including six B. anthracis strains were identified correctly.

232 and dynamic range were determined by spiking B. anthracis DNA into individual PCR mixtures and B. ant

233 s rapidly, subsequent and frequent sublethal B. anthracis infections cause maturation of anti-anthrax

234 matured less well in response to subsequent B. anthracis peptidoglycan (Ba PGN) exposure, with reduc

235 esign of inhibitors that specifically target B. anthracis and other microbial IMPDH enzymes.

236 rmis PGA both elicited more TLR2 signal than B. anthracis PGA, but only responses to B. subtilis PGA

237 eniformis PGA elicited more TLR4 signal than B. anthracis PGA, whereas B. subtilis PGA elicited none.

238 We conclude that B. anthracis PGA is recognized less effectively by innat

239 Our findings demonstrate that B. anthracis has evolved to use LT and ET to induce host

240 We found that B. anthracis and C. tetani epitopes were the most promis

241 We have shown previously that B. anthracis Sterne is capable of blood-brain barrier (B

242 Our results show that B. anthracis LT blunts signaling through Tie-2, thereby

243 Previous work has shown that B. anthracis spores use germination (Ger) receptors to r

244 Together, the results suggest that B. anthracis spores have special properties that promote

245 The B. anthracis regulon includes homologues of some B. subt

246 ch are necessary for SLH domains to bind the B. anthracis SCWP.

247 er reaction and 10 CFU/ml blood for both the B. anthracis Sterne and V1B strains.

248 by specific detection of Sap secreted by the B. anthracis in culture broth just after 1h of growth.

249 ce proteins attached to the cell wall by the B. anthracis Sortase A ((Ba)SrtA) enzyme.

250 In contrast, the B. anthracis lcpB3 variant displayed reduced cell size a

251 parvum IMPDH inhibitors was examined for the B. anthracis enzyme and compared with those of three bac

252 In this study, we identified the B. anthracis lcpD mutant, which displays increased chain

253 malian substrates but also by modulating the B. anthracis secretome itself.

254 ontrast to hitherto characterized NrdIs, the B. anthracis NrdI is stable in its semiquinone form (Nrd

255 were sequenced and compared with that of the B. anthracis Ames ancestor, the progenitor of all B. ant

256 s well as BslO near the septal region of the B. anthracis envelope.

257 Here the transmembrane topologies of the B. anthracis GerH(A), GerH(B), and GerH(C) proteins are

258 In solving the crystal structure of the B. anthracis siderophore biosynthesis protein B (AsbB),

259 gene immediately downstream of secA2 on the B. anthracis chromosome, is also a determinant of chain

260 Here, we report the effect of InhA1 on the B. anthracis secretome.

261 dily form biofilms, we hypothesized that the B. anthracis sinIR regulon is distinct from that of B. s

262 inkage units tethers pyruvylated SCWP to the B. anthracis envelope, thereby enabling S-layer assembly

263 erminal domain having some similarity to the B. anthracis septum site-determining protein MinD and a

264 he responses of human innate immune cells to B. anthracis PGA and PGAs from nonpathogenic B. subtilis

265 molecular mechanisms of PHB contribution to B. anthracis sporulation and provide valuable insight in

266 nd therapeutic avenues for humans exposed to B. anthracis.

267 and can partially booster their immunity to B. anthracis.

268 ew synthesizes the advances made relative to B. anthracis spore decontamination science and technolog

269 (SNP) previously reported to be specific to B. anthracis was detected in some B. cereus strains.

270 on 1139, was identified as being specific to B. anthracis, which is a biothreat agent with high morta

271 ficient mice had increased susceptibility to B. anthracis and anthrax lethal toxin but not to edema t

272 e challenged with nonencapsulated, toxigenic B. anthracis or with anthrax toxins.

273 However, besides toxins, B. anthracis expresses effector proteins, whose role in

274 ed PCR assay for detection of F. tularensis, B. anthracis, and Y. pestis directly from patient blood

275 Deltasap mutant in trans with the wild-type B. anthracis sap or the sap gene from either of two diff

276 Unlike B. anthracis, much of the increased virulence gene expre

277 the disease pathophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mut

278 ted antimicrobial effects against vegetative B. anthracis bacilli.

279 er in their efficiency of recovery of viable B. anthracis cells.

280 portantly, lethal toxin produced by virulent B. anthracis blocked activation of protein kinases, p38

281 IL-1-dependent host protection from virulent B. anthracis.

282 s monkeys challenged with the fully virulent B. anthracis Ames wild-type strain or the isogenic toxin

283 ntratracheal spore challenge by the virulent B. anthracis Ames strain.

284 Swabs were spiked with virulent B. anthracis cells, and the methods were compared for th

285 The West African Group (WAG) B. anthracis have mutations rendering them anthrose defi

286 is most lethal and of greatest concern when B. anthracis is weaponized.

287 We propose a model whereby B. anthracis LCPs promote attachment of SCWP precursors

288 Here, we investigated whether B. anthracis impacts the function of colonic B-1 cells t

289 vide new insight into the mechanism by which B. anthracis triggers sepsis during a critical stage of

290 thrax; however, the mechanisms through which B. anthracis-derived factors contribute to the pathology

291 bserved for F. tularensis when compared with B. anthracis while the observed profiles of each of the

292 EF in liver lysates from mice infected with B. anthracis Sterne 34F2.

293 IgM MAb to A/JCr mice lethally infected with B. anthracis strain Sterne had no significant effect on

294 induced genes in a macrophage infected with B. anthracis.

295 survival following intranasal infection with B. anthracis spores in our studies but significantly inc

296 Acute infection with B. anthracis Sterne and the DeltaLF mutant resulted in d

297 ere completely protected from infection with B. anthracis strain Sterne, which suggested that a polyc

298 that weeks after intranasal inoculation with B. anthracis spores, substantial amounts of spores could

299 ) responded differentially to the PGAs, with B. anthracis PGA being least stimulatory and B. lichenif

300 ng of Cry5B-expressing B. thuringiensis with B. anthracis can result in lethal infection of C. elegan