ライフサイエンスコーパス: anthrax

1 other well-studied heptameric toxins (i.e., anthrax).

2 t Bacillus anthracis infection, the agent of anthrax.

3 ere originally submitted for tests to detect anthrax.

4 pore-forming gram-positive bacterium, causes anthrax.

5 a potential therapeutic for the treatment of anthrax.

6 a life-saving, postexposure therapy against anthrax.

7 arget for the diagnosis and the treatment of anthrax.

8 nthracis spores causes gastrointestinal (GI) anthrax.

9 f Bacillus anthracis, the causative agent of anthrax.

10 se of 10(4)B. anthracis cells for inhalation anthrax.

11 Bacillus anthracis can cause inhalational anthrax.

12 ll mutant is avirulent in a murine model for anthrax.

13 f Bacillus anthracis, the causative agent of anthrax.

14 of all common manifestations of the disease anthrax.

15 prominent clinical manifestation of systemic anthrax.

16 n Bacillus anthracis, the causative agent of anthrax.

17 herapeutic VNAs and/or diagnostic agents for anthrax.

18 Inhalational anthrax, a disease caused by inhaling Bacillus anthracis

19 In a mouse model for anthrax, a HPr(-) EI(-) mutant was attenuated for virule

20 llus anthracis spores initiates inhalational anthrax, a life-threatening infection.

21 ity of elephants and springbok to mount anti-anthrax adaptive immune responses is still equivocal, ou

22 of bacilli from the thoracic cavity to cause anthrax after inhalation challenge with spores.

23 Bacillus anthracis, the anthrax agent, is a member of the Bacillus cereus sensu

24 ing, Gram-positive bacterium responsible for anthrax, an acute infection that most significantly affe

25 ive bacterium that is the causative agent of anthrax and a potential weapon of bioterrorism.

26 es that target events in the pathogenesis of anthrax and may potentially augment antimicrobials are b

27 , and polio, and biological threats, such as anthrax and plague.

28 nti-protective antigen antibodies to prevent anthrax and suggest that lethal factor is the dominant t

29 ich serves as a simulant of B. anthracis (or anthrax) and which possesses a peptidoglycan (sugar)-ric

30 nst Shiga, botulinum, Clostridium difficile, anthrax, and ricin toxins.

31 ith other computation models of inhalational anthrax, and using the resulting information towards ext

32 -linked immunosorbent assays to measure anti-anthrax antibody titres and developed three increasingly

33 k and 3-52% of elephants had measurable anti-anthrax antibody titres, depending on the model used.

34 ible human risk assessments for inhalational anthrax associated with exposure to a low number of bact

35 ential adjunctive agents in the treatment of anthrax-associated shock.

36 plays a central role in the pathogenesis of anthrax-associated shock.

37 asive and received a final stimulus when the anthrax attack occurred in the United States in 2001.

38 Japanese religious cult sought to launch an anthrax attack on Tokyo.

39 en a top bioterrorism concern since the 2001 anthrax attacks in the USA.

40 determined by testing blood spiked with non-anthrax bacterial isolates or by testing blood samples d

41 of exposure to lethal concentrations of the anthrax bacterium, Bacillus anthracis, for grazing anima

42 e to category BSL 3 and 4 pathogens, such as anthrax, bubonic plague, Ebola and Marburg fever.

43 vity against Gram-positive bacteria, such as anthrax, but also shows activity against selected Gram-n

44 apsule may contribute to the pathogenesis of anthrax by suppressing the responses of immune cells and

45 h Bacillus anthracis, the causative agent of anthrax, can lead to persistence of lethal secreted toxi

46 ly important sapronoses, such as cholera and anthrax, can sustain an epidemic in a host population.

47 We follow pathogen concentrations at anthrax carcass sites and waterholes for five years and

48 ng the terminal diversity of B. anthracis in anthrax carcasses.

49 sified 95% (95% CI, 93% to 97%) of 353 adult anthrax case patients and 76% (CI, 73% to 79%) of 647 co

50 to 100%), respectively, when only inhalation anthrax cases or higher-quality case reports were invest

51 Here we show that the dynamics of an anthrax-causing agent, Bacillus cereus biovar anthracis,

52 ivity, and is selectively active against the anthrax-causing organism.

53 d may be used as a safe oral vaccine against anthrax challenge.

54 easily at high protonation state through the anthrax channel (and the varphi clamp), the initial perm

55 l factor (LF) N-terminal segment through the anthrax channel.

56 sperm protamine, that effectively inhibited anthrax cytotoxic protease and demonstrated that they al

57 demonstrated that the course of inhalational anthrax disease and the resulting pathology in guinea pi

58 g bacterium Bacillus anthracis causes lethal anthrax disease in humans and animals.

59 pores that upon germination can cause lethal anthrax disease in humans.

60 the course and manifestation of experimental anthrax disease induced under controlled conditions in t

61 Anthrax disease is caused by a toxin consisting of prote

62 significant importance with respect to both anthrax disease progression, spore detection for biodefe

63 Bacillus anthracis, the etiological agent of anthrax disease, as the model pathogen.

64 Bacillus anthracis, the causative agent of anthrax disease, is lethal owing to the actions of two e

65 Bacillus anthracis is the causative agent of anthrax disease, presents with high mortality, and has b

66 T) domains and its efficacy as a vaccine for anthrax disease.

67 and lipid mediators in host survival during anthrax disease.

68 er proteins with known or potential roles in anthrax disease.

69 dG renders B. anthracis incapable of causing anthrax disease.

70 Bacillus anthracis, the causative agent of anthrax, displays a remarkable ability to grow in mammal

71 cellent levels of detection and accuracy for anthrax DNA can be achieved using PNA probes with suitab

72 Despite this, our current knowledge of anthrax ecology is largely limited to arid ecosystems, w

73 alysis by the adenylyl cyclase domain of the anthrax edema factor toxin was simulated using the empir

74 get, mitogen-activated protein kinase 1, and anthrax edema toxin fails to increase intracellular cycl

75 understood, despite multi-decade research on anthrax epizootic and epidemic dynamics; many countries

76 tform, particularly for vaccines such as for anthrax, for which rapid induction of protective immunit

77 Bacillus anthracis, the causative agent of anthrax, forms an S-layer atop its peptidoglycan envelop

78 covering symptoms and signs can distinguish anthrax from other conditions with minimal need for diag

79 Biological weapons such as smallpox and anthrax had the potential to cause a national catastroph

80 nthracis infections cause maturation of anti-anthrax immunity.

81 such as Bacillus anthracis, causal agent of anthrax in humans and animals.

82 rrently U.S. FDA-approved vaccine to prevent anthrax in humans is anthrax vaccine adsorbed (AVA), whi

83 rats, and 24-hour postprophylaxis of inhaled anthrax in mice.

84 d toxins in the pathogenesis of inhalational anthrax in rabbits by comparing infection with the Ames

85 efficacy of medical countermeasures against anthrax in support of licensure under the FDA's "Animal

86 As physicians involved in diagnosing anthrax in the index case and alerting authorities, we o

87 thophysiology, and pathology of inhalational anthrax in this animal model following nose-only aerosol

88 y to confer post-exposure protection against anthrax in vivo.

89 opathologic findings typical of disseminated anthrax included suppurative (heterophilic) inflammation

90 In vivo, we found that 100% of anthrax-infected rabbits survived when treated with cAb2

91 o investigate risk factors in an outbreak of anthrax infection among Scottish heroin users.

92 xtravascular fluid collection characterizing anthrax infection clinically.

93 Furthermore, in a murine anthrax infection model, 15d-PGJ2 reversed anthrax letha

94 r methicillin-resistant S. aureus (MRSA) and anthrax infection, respectively.

95 both pathways is likely necessary for lethal anthrax infection.

96 mproved survival of mice in a spore model of anthrax infection.

97 nd their roles in initial and late stages of anthrax infection.

98 virulence in a murine model of inhalational anthrax infection.

99 vaccine component and therapeutic target for anthrax infections but also an excellent model system fo

100 Fatal, natural anthrax infections transmit the bacterium through new ho

101 oninvasive method to explore the dynamics of anthrax infections, by evaluating the terminal diversity

102 te that zebra in ENP often survive sublethal anthrax infections, encounter most B. anthracis in the w

103 acis, the bacterial pathogen responsible for anthrax infections.

104 els of leak-associated infections, including anthrax, influenza, malaria, and sepsis.

105 ive tool for the analysis of the kinetics of anthrax intoxication and ultimately drug discovery.

106 et spore germination or downstream events in anthrax intoxication are also under investigation.

107 Anthrax is a globally important animal disease and zoono

108 Anthrax is a life-threatening disease caused by infectio

109 over three decades, we show that rainforest anthrax is a persistent and widespread cause of death fo

110 Despite the fact that anthrax is an ancient and emerging zoonotic infectious d

111 The ability of B. anthracis to cause anthrax is attributed to the plasmid-encoded A/B-type to

112 Inhalational anthrax is caused by inhalation of Bacillus anthracis sp

113 Anthrax is caused by the spore-forming, gram-positive ba

114 Gastrointestinal (GI) anthrax is the most prevalent form of naturally acquired

115 The infectious agent of the disease anthrax is the spore of Bacillus anthracis.

116 Bacillus anthracis, the causative agent of anthrax, is a potential bioterrorism agent.

117 Bacillus anthracis, the causative agent of anthrax, is a well known bioterrorism agent.

118 Bacillus anthracis, the etiological agent of anthrax, is a well-established model organism.

119 GI anthrax led to significant inhibition of immunoglobulins

120 tigen (PA) is essential for the transport of anthrax lethal and edema toxins into human cells.

121 an anti-cancer fusion protein consisting of anthrax lethal factor (LF) and the catalytic domain of P

122 Anthrax lethal factor (LF) enters the cytosol through po

123 The metalloproteinase anthrax lethal factor (LF) is secreted by Bacillus anthr

124 Anthrax lethal factor (LF) is then able to translocate t

125 ensin RTD-1 is a noncompetitive inhibitor of anthrax lethal factor (LF) protease (IC50 = 390 +/- 20 n

126 Certhrax shares 31% sequence identity with anthrax lethal factor from Bacillus anthracis; however,

127 Finally, the pathogen's anthrax lethal factor is required to establish lethal in

128 The anthrax lethal factor metalloprotease and small-molecule

129 crophages pre-exposed to a sublethal dose of anthrax lethal toxin (LeTx) are refractory to subsequent

130 ages expressing a functional NLRP1b prevents anthrax lethal toxin (LeTx)-induced caspase-1 autoproteo

131 his BaPGN-induced response was suppressed by anthrax lethal toxin (LT) and edema toxin (ET), with the

132 ethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET).

133 The anthrax lethal toxin (LT) enters host cells and enzymati

134 Anthrax lethal toxin (LT) is a protease virulence factor

135 Anthrax lethal toxin (LT) is an A-B type toxin secreted

136 Anthrax lethal toxin (LT), produced by Bacillus anthraci

137 These two proteins combine to form anthrax lethal toxin (LT), whose proximal targets are mi

138 pathology associated with administration of anthrax lethal toxin (LT).

139 Anthrax lethal toxin and edema toxin, which are composed

140 required for two very different toxins: the anthrax lethal toxin and the pore-forming toxin aerolysi

141 We find that anthrax lethal toxin fails to cleave its target, mitogen

142 indicate that radiolabeled forms of mutated anthrax lethal toxin hold promise for noninvasive imagin

143 ome is activated upon direct cleavage by the anthrax lethal toxin protease.

144 Engineered tumor-targeted anthrax lethal toxin proteins have been shown to strongl

145 ype protective antigen (PA-WT) of the binary anthrax lethal toxin was modified to form a pore in cell

146 and also reduces the detrimental effects of anthrax lethal toxin, diphtheria toxin, cholera toxin, P

147 omes by their respective activating signals, anthrax lethal toxin, nigericin, and flagellin.

148 ed to activate NLRP1 and/or CARD8, including anthrax lethal toxin, Toxoplasma gondii, Shigella flexne

149 screen to identify host factors required for anthrax lethal toxin-induced cell death.

150 provided almost complete protection against anthrax lethal toxin-induced cytotoxicity and death in m

151 provided protection against NLRP1-dependent anthrax lethal toxin-mediated cell death and prevented N

152 e anthrax infection model, 15d-PGJ2 reversed anthrax lethal toxin-mediated NLRP1-dependent resistance

153 sufficient to confer macrophage survival to Anthrax lethal toxin.

154 th specific antibody prior to treatment with anthrax lethal toxin.

155 th specific antibody prior to challenge with anthrax lethal toxin.

156 d increased the survival of cells exposed to anthrax lethal toxin.

157 ated with the NALP1b inflammasome activator, anthrax lethal toxin.

158 all molecules was screened for inhibitors of anthrax lethal toxin.

159 flammasome activation by either flagellin or anthrax lethal toxin.

160 One of these sensors, NLRP1, detects anthrax lethal toxin; however, the mechanism of NLRP1 ac

161 016 Zika pandemic, 2014 Ebola outbreak, 2001 anthrax letter attacks, and 1984 Rajneeshee Salmonella a

162 anthracis spores made after one of the 2001 anthrax letter attacks.

163 ion may also protect humans from respiratory anthrax-like death.

164 XO1-like virulence plasmid cause respiratory anthrax-like disease in humans, particularly in welders.

165 As the pathogenesis of B. cereus anthrax-like disease in mice is dependent on pagA1 and P

166 eus G9241 contributes to the pathogenesis of anthrax-like disease in mice.

167 that had been isolated from a fatal case of anthrax-like disease.

168 ver, some recent isolates cause inhalational anthrax-like diseases and death.

169 ereus strains and enable the pathogenesis of anthrax-like diseases.

170 Bacillus cereus G9241, which caused an anthrax-like infection, has two virulence plasmids, pBCX

171 screening patients for meningitis during an anthrax mass casualty incident.

172 re essential for successful management of an anthrax mass casualty incident.

173 d as a 4-item assessment tool for use during anthrax mass casualty incidents.

174 of 363 (36%) cases with systemic anthrax met anthrax meningitis criteria.

175 Anthrax meningitis is a common manifestation of B. anthr

176 r on admission had a sensitivity for finding anthrax meningitis of 89% (83%) in the adult (pediatric)

177 Survival of anthrax meningitis was predicted by treatment with a bac

178 Anthrax meningitis was unlikely in the absence of any of

179 inical diagnostic and prognostic factors for anthrax meningitis.

180 thirty-two of 363 (36%) cases with systemic anthrax met anthrax meningitis criteria.

181 ined from immunized alpacas and screened for anthrax neutralizing activity in macrophage toxicity ass

182 , rather than being solely a lethal disease, anthrax often occurs as a sublethal infection in some su

183 of a model ligand, the protective antigen of anthrax on the gold surface, is monitored in real-time w

184 Widespread release of Bacillus anthracis (anthrax) or Yersinia pestis (plague) would prompt a publ

185 entified an anthrose-deficient strain in the anthrax outbreak among European heroin users.

186 ch as the Amerithrax incident of 2001 or the anthrax outbreaks in Russia and Sweden in 2016, critical

187 nce dataset of human, livestock and wildlife anthrax outbreaks.

188 of the Bacillus cereus group, including the anthrax pathogen, contains a 2D-crystalline basal layer,

189 The genes for anthrax pathogenesis are located on two large virulence

190 nea pig, which has been used extensively for anthrax pathogenesis studies and anthrax vaccine potency

191 elegans is a useful infection model to study anthrax pathogenesis.

192 obust host response, which may contribute to anthrax pathogenesis.

193 pecificity and efficiency of the re-directed anthrax pore for transport of TccC3 toxin and establishe

194 fforts for wild ungulates that coincide with anthrax-prone landscapes.

195 (mAb) sandwich pair for the detection of an anthrax protective antigen (PA(83)).

196 Following assembly, the anthrax protective antigen (PA) forms an oligomeric tran

197 he sensitive, specific and easy detection of anthrax protective antigen (PA) toxin in picogram concen

198 gh pores in the endosomal membrane formed by anthrax protective antigen.

199 Activation of PA-L1 in vitro correlated with anthrax receptor expression and MMP activity (HT1080 > M

200 diated activation of PA-L1 was correlated to anthrax receptor expression and MMP activity in a panel

201 A; mPA) which cannot bind to the two natural anthrax receptors.

202 nc hydrolase that is chiefly responsible for anthrax-related cell death.

203 Bacillus anthracis, the causative agent of anthrax, relies on multiple virulence factors to subvert

204 Bacillus anthracis, the causative agent of anthrax, replicates as chains of vegetative cells by reg

205 We conclude by mapping where anthrax risk could disrupt sensitive conservation effort

206 ): 0.59-4.16 billion) live within regions of anthrax risk, but most of that population faces little o

207 distribution of B. anthracis as a proxy for anthrax risk.

208 Rapid identification of patients needing anthrax-specific therapies will improve patient outcomes

209 JMO-G1, was fully protective against lethal anthrax spore infection in mice as a single dose.

210 Anthrax spores can be aerosolized and dispersed as a bio

211 ted from challenge with 200 LD50 aerosolized anthrax spores.

212 Working in the natural anthrax system of Etosha National Park, Namibia, we coll

213 ly more zebras responding immunologically to anthrax than have previous studies using less comprehens

214 f entry for Bacillus anthracis in inhalation anthrax, the deadliest form of the disease.

215 s, our studies show the potential of VNAs as anthrax therapeutics.

216 rming bacterium, is such a pathogen, causing anthrax through a combination of bacterial infection and

217 tive activity against the causative agent of anthrax toxicity.

218 As anthrax toxin (Atx) accesses the cytosol, the purpose of

219 e detection of B. anthracis by using atxA an anthrax toxin activator gene.

220 ate talin-1 are exploited for association of anthrax toxin and its principal receptor, CMG2, with hig

221 ture and function of Tc toxins with those of anthrax toxin and vertebrate teneurin.

222 encodes a host membrane protein exploited by anthrax toxin as a principal receptor, dramatically alte

223 doing so we targeted a protease component of anthrax toxin as well as host proteases exploited by thi

224 ages and human lymphoblastoid cells affected anthrax toxin binding, internalization, and sensitivity.

225 The protective antigen (PA) moiety of anthrax toxin binds to cellular receptors and mediates t

226 tency in cell assays and protected mice from anthrax toxin challenge with much better efficacy than t

227 e cleaved by LF show a greater resistance to anthrax toxin challenge.

228 ways to the neutralizing activity of an anti-anthrax toxin chimeric mAb.

229 The impact of ZDHHC5 on Furin/PC7-mediated anthrax toxin cleavage is dual, having an indirect and a

230 on-antimicrobial drugs with activity against anthrax toxin components; and agents that inhibit bindin

231 The tripartite anthrax toxin consists of protective antigen, lethal fac

232 Protective antigen of anthrax toxin forms a pore through which the two catalyt

233 Anthrax toxin forms one such machine through the self-as

234 regulator AtxA controls transcription of the anthrax toxin genes and capsule biosynthetic operon.

235 ing the protective antigen (PA) component of anthrax toxin genetically fused to a dendritic cell (DC)

236 e polypeptide-based polyvalent inhibitors of anthrax toxin in which multiple copies of an inhibitory

237 Anthrax toxin is a tripartite virulence factor produced

238 Anthrax toxin is an intracellularly acting toxin in whic

239 Anthrax toxin is an intracellularly acting toxin where s

240 Anthrax toxin is composed of three proteins, a transloca

241 er as a fusion to the N-terminal fragment of anthrax toxin lethal factor or when naturally delivered

242 We generated anti-anthrax toxin mAbs with specific Fc domain variants with

243 engagement, with minimal protection against anthrax toxin observed in FcgammaR-deficient mice follow

244 molysin pore from Staphylococcus aureus, the anthrax toxin pore and the 1.2-MDa mouse mechanosensitiv

245 and that this change is sufficient to affect anthrax toxin production.

246 Anthrax toxin protective antigen (PA) delivers its effec

247 ure supernatant directly cleaved each of the anthrax toxin proteins as well as an additional secreted

248 Here, we have identified anthrax toxin receptor 1 (ANTXR1) as the receptor for SV

249 The anthrax toxin receptor 1 (ANTXR1) has been identified as

250 this corresponded with the higher levels of anthrax toxin receptor 1 (ANTXR1) in these cells than in

251 r endothelial marker 8 (TEM8), also known as anthrax toxin receptor 1 (ANTXR1), is a highly conserved

252 tasis of other membrane proteins as CFTR and anthrax toxin receptor 2, two poor folders involved in s

253 olipoprotein A-IV], CLU [clusterin], ANTRX2 [anthrax toxin receptor 2], PON1 [serum paraoxonase/aryle

254 Here we generated cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2

255 ls would be protected from anthrax toxins if anthrax toxin receptor expression was effectively silenc

256 Thus, anthrax toxin receptor-targeted RNAi has the potential t

257 lular matrix binding protein that is also an anthrax toxin receptor.

258 Thus, anthrax toxin receptors in mouse and human macrophages w

259 nthrax toxins enter cells via two identified anthrax toxin receptors: tumor endothelial marker 8 (TEM

260 e pathways does not explain the lethality of anthrax toxin(1,2).

261 nd edema factor, which are the components of anthrax toxin, and other proteins with known or potentia

262 Anthrax toxin, comprising protective antigen, lethal fac

263 Anthrax toxin, comprising three proteins-protective anti

264 acis protective antigen (PA), a component of anthrax toxin, results in significantly augmented protec

265 B. cereus strain G9241 expresses anthrax toxin, several polysaccharide capsules, and the

266 nhanced the in vitro and in vivo activity of anthrax toxin-neutralizing antibodies.

267 to be ineffective against strains that lack anthrax toxin.

268 ive antigen (PA(63)) component of the binary anthrax toxin.

269 oylation is required for the cleavage of the anthrax toxin.

270 antigen (PA), the cell-binding component of anthrax toxin.

271 terium's major virulence factors are (a) the anthrax toxins and (b) an antiphagocytic polyglutamic ca

272 ltaatxA1 mutant produced lower levels of the anthrax toxins and no hyaluronic acid capsule.

273 This review focuses on the activities of anthrax toxins and their roles in initial and late stage

274 ter stages of infection, when high levels of anthrax toxins are present.

275 The anthrax toxins are three polypeptides-protective antigen

276 We also showed that the anthrax toxins did not play a role in persistence.

277 Anthrax toxins enter cells via two identified anthrax to

278 ized that host cells would be protected from anthrax toxins if anthrax toxin receptor expression was

279 This review focuses on the role of anthrax toxins in pathogenesis.

280 aracterized a new set of 15 VHHs against the anthrax toxins that act by binding to the edema factor (

281 inst the protective antigen component of the anthrax toxins.

282 g-targeted pathology would be beneficial for anthrax treatment.

283 Certhrax resides in the mART domain, whereas anthrax uses a metalloprotease mechanism.

284 d as an adjuvant for a candidate vaccine for anthrax using recombinant protective Ag (rPA) from Bacil

285 tant of a nonencapsulated, toxigenic strain (anthrax vaccine absorbed [AVA]) whose primary protective

286 Anthrax vaccine adsorbed (AVA) immunization raised antib

287 oved vaccine to prevent anthrax in humans is anthrax vaccine adsorbed (AVA), which is protective in s

288 healthy subjects following immunization with Anthrax Vaccine Adsorbed (AVA).

289 The U.S.-licensed anthrax vaccine is made from an incompletely characteriz

290 nsively for anthrax pathogenesis studies and anthrax vaccine potency testing, is a good candidate for

291 ered in the development of a next-generation anthrax vaccine.

292 Improving next-generation anthrax vaccines is important to safeguard citizens and

293 sired characteristic of vaccines, especially anthrax vaccines, which must be stockpiled for large-sca

294 (rPA)--the major component of new-generation anthrax vaccines--affects vaccine immunogenicity, we cre

295 Though we found that adaptive immunity to anthrax wanes rapidly, subsequent and frequent sublethal

296 er understand the pathogenesis of DIC during anthrax, we compared the effects of 24-hour infusions of

297 del appeared to describe rabbit inhalational anthrax well.

298 sks (CR) computational model of inhalational anthrax where data was collected from NZW rabbits expose

299 enge of guinea pigs resulted in inhalational anthrax with death occurring between 46 and 71 h postcha

300 and requires more aggressive treatment than anthrax without meningitis.