ライフサイエンスコーパス: C. perfringens

1 C. perfringens and B. fragilis provided moderate synergy

2 C. perfringens beta toxin (CPB) is the major virulence d

3 C. perfringens EtfA was expressed in and purified from E

4 C. perfringens is an underrecognized but frequently obse

5 C. perfringens is responsible for a wide spectrum of dis

6 C. perfringens lacks flagella but possesses type IV pili

7 C. perfringens sleC spores did not germinate completely

8 C. perfringens spores are thought to be the important in

9 C. perfringens spores lacking GerO were defective in ger

10 C. perfringens survival in the presence of mouse periton

11 C. perfringens type A strains producing C. perfringens e

12 C. perfringens type C isolates, which cause rapidly fata

13 C. perfringens, an opportunistic pathogen, was specifica

14 nvestigate genotypic relationships among 139 C. perfringens isolates from 74 flocks.

15 e carried out whole-genome sequencing of 272 C. perfringens isolates from 70 infants across 5 hospita

16 A C. perfringens strain with etfA inactivated is blocked i

17 e secreted by Clostridium perfringens, and a C. perfringens hyaluronidase nagI or nagK pseudogene wer

18 levels and the amount of CPB2 produced by a C. perfringens cell and that decreased transcription and

19 ight regulate the pathogenicity of CN3685, a C. perfringens type C strain.

20 arrying a chromosomal cpe gene) and F4969 (a C. perfringens type A non-food-borne GI disease isolate

21 antiserum screen of mutants generated from a C. perfringens transposon-mutant library, here we identi

22 s, we investigated whether the cpe gene of a C. perfringens food poisoning isolate can be expressed a

23 on by SM101, a transformable derivative of a C. perfringens food-poisoning strain.

24 genetic element near the dcm sequences of a C. perfringens plasmid.

25 out mutants in both SM101 (a derivative of a C. perfringens type A food poisoning isolate carrying a

26 ota toxin genes, to several different type A C. perfringens isolates.

27 esults allow the following conclusions about C. perfringens spore germination: (i) SleC is essential

28 ing the production of NanI, which may affect C. perfringens growth, adhesion, and toxin binding in vi

29 Biofilms afforded C. perfringens protection from environmental stress, inc

30 ding of Ib was inhibited by antisera against C. perfringens type E or Clostridium spiroforme culture

31 e of macrophages in the host defense against C. perfringens infections is still unknown.

32 tory concentration (MIC) of 3.288 uM against C. perfringens, comparable with other antimicrobial pept

33 No effective vaccine against C. perfringens is currently available.

34 are among the most plasmid dependent of all C. perfringens isolates for virulence, as they usually c

35 . albicans into "mini-biofilms," which allow C. perfringens cells to survive in a normally toxic envi

36 Although C. perfringens strains form biofilm-like structures, the

37 ontal transfer of a common cpe plasmid among C. perfringens type A strains.

38 rane-active toxins produced by the anaerobic C. perfringens, alpha-toxin (PLC) and perfringolysin O (

39 Enterococci and C. perfringens, but not E. coli, showed significantly sm

40 Mucolytic bacteria in general and C. perfringens in particular were selected when enteral

41 developmental stage, sampling location, and C. perfringens.

42 Sequential Eimeria maxima and C. perfringens challenges significantly induced NE, seve

43 this sense, novel biopreservatives with anti-C. perfringens activity are of interest.

44 No PG-associated and NE-associated C. perfringens isolates shared the same sequence type or

45 le in the core genomes of poultry-associated C. perfringens isolates, a concept with both epidemiolog

46 omology to pilins in Gram-negative bacteria, C. perfringens appears to have two pilin subunits, PilA1

47 udies have recently indicated a link between C. perfringens and the preterm infant disease necrotizin

48 rfringens type A food poisoning is caused by C. perfringens isolates carrying a chromosomal cpe gene,

49 nificantly reduce the impact of NE caused by C. perfringens on broilers.

50 al gastrointestinal (GI) illnesses caused by C. perfringens type A isolates, including C. perfringens

51 iarrhea and gas gangrene, that are caused by C. perfringens.

52 ns of food-borne-disease outbreaks caused by C. perfringens.

53 Amino acid conjugation by C. perfringens BSH/T was diverse, including all proteina

54 The same four sigma factors are encoded by C. perfringens genomes, and two (SigE and SigK) have pre

55 nscriptional regulation of CPE expression by C. perfringens food poisoning isolates.

56 Finally, when samples were grouped by C. perfringens virulence factors, we found dramatic chan

57 , when activated in a dysregulated manner by C. perfringens alpha toxin, may contribute to localized

58 encoded alpha-toxin and perfringolysin O by C. perfringens, as well as sporulation by Clostridium bo

59 de for the alpha and beta toxins produced by C. perfringens.

60 ortedly control in vitro toxin production by C. perfringens but their importance for virulence has no

61 ly for other LCTs and for TpeL production by C. perfringens strain JIR12688.

62 gene, which encodes a sialidase secreted by C. perfringens, in the M. alligatoris genome.

63 ader sequence necessary for its secretion by C. perfringens is absent.

64 is a catabolite repressor of sporulation by C. perfringens.

65 occurrence of outbreaks caused by B. cereus, C. perfringens, and S. aureus in the United States.

66 - 0.02), microbial quality (against E. coli, C. perfringens, lactic acid bacteria, psychrophilic bact

67 which codes for beta-glucuronidase; E. coli-C. perfringens shuttle vectors carrying the fusions were

68 the tcp genes, which can mediate conjugative C. perfringens plasmid transfer.

69 tential as a biopreservative for controlling C. perfringens in food.

70 ly, we observed that in suspension cultures, C. perfringens induces aggregation of C. albicans into "

71 ed carriage of the tpeL gene among different C. perfringens strains, detecting this toxin gene in som

72 lation of sporulation varies among different C. perfringens strains.

73 d only in the mother cell compartment during C. perfringens sporulation.

74 ential synergistic toxin interactions during C. perfringens intestinal infections and support a possi

75 ncerted action of alpha-toxin and PFO during C. perfringens pathogenesis.

76 2+) and DPA into the developing spore during C. perfringens sporulation.

77 or Ca-DPA uptake by developing spores during C. perfringens sporulation.

78 rrying sequences for the gene (cpe) encoding C. perfringens enterotoxin (CPE), were unable to express

79 od poisoning, is produced by enterotoxigenic C. perfringens type A isolates when these bacteria sporu

80 nsformants and the naturally enterotoxigenic C. perfringens NCTC 8239 were similar and that this mess

81 The enzyme C. perfringens neuraminidase (CpNA) removes sialic acid

82 However, many EN strains also express C. perfringens enterotoxin (CPE), suggesting that CPE co

83 Although they lack flagella, C. perfringens bacteria can still migrate across surface

84 demonstrated that tissue destruction follows C. perfringens phospholipase C (PLC)-induced, platelet g

85 Sporulation is critical for C. perfringens type A food poisoning since spores contri

86 oxin) is the major virulence determinant for C. perfringens type-A food poisoning, the second most co

87 ative sigma factors, which are essential for C. perfringens sporulation.

88 s a potential auxiliary virulence factor for C. perfringens enteritis and enterotoxemia.

89 studies can be applied to in vivo models for C. perfringens growth and metabolism of mucin O-glycans,

90 alternative sigma factors are necessary for C. perfringens sporulation, but only SigE, SigF, and Sig

91 uity of the patient's bowel was negative for C. perfringens.

92 eins and Ca-DPA release are not required for C. perfringens spore germination.

93 perfringens isolates may be responsible for C. perfringens type A food poisoning versus CPE-associat

94 se observations support a potential role for C. perfringens in NMO pathogenesis.

95 However, the importance of SigF and SigG for C. perfringens sporulation or CPE production had not yet

96 a toxin, which are also important toxins for C. perfringens diseases (enteritis and enterotoxemia) or

97 A 4.0-kb DNA fragment from C. perfringens NCTC 8798 that contains the nanE and nanA

98 , from the genomic DNA library prepared from C. perfringens ATCC10543.

99 Upon its release from C. perfringens spores, CPE binds to its receptor, claudi

100 tream and downstream flanking sequences from C. perfringens food poisoning isolate NCTC 8239, or a 1.

101 nd all genes examined from M. gallisepticum, C. perfringens, and S. pneumoniae were under neutral to

102 We successfully detected and genotyped C. perfringens in tissue sections from two autopsy cases

103 Less than 5% of the global C. perfringens population apparently carries the cpe gen

104 the diarrheal and cramping symptoms of human C. perfringens type A food poisoning.

105 food samples and, until recently, identified C. perfringens to the species level only.

106 These findings implicate C. perfringens TFP in the ability of C. perfringens to a

107 he sequential production of DHDPA and DPA in C. perfringens appears to be catalysed by DHDPA synthase

108 mutagenesis system that works effectively in C. perfringens.

109 hways through which virulence has evolved in C. perfringens.

110 Thus, CpAL regulates biofilm formation in C. perfringens by increasing levels of certain toxins re

111 ribosomal methylase B (ermB) gene - found in C. perfringens and C. difficile.

112 ption and translation of the spoIIID gene in C. perfringens were not affected by mutations in sigE an

113 regulating the expression of other genes in C. perfringens.

114 n, suggesting an auxiliary role for GerAA in C. perfringens spore germination.

115 r poultry dishes were commonly implicated in C. perfringens (63%) and S. aureus (55%) outbreaks, and

116 eron and that transcription of the operon in C. perfringens is inducible by the addition of sialic ac

117 ureus outbreaks (median, 87%), but rarely in C. perfringens outbreaks (median, 9%).

118 valent cation transporters play some role in C. perfringens spore germination.

119 pA is necessary for efficient sporulation in C. perfringens, glucose-mediated catabolite repression o

120 tment in which enterotoxin is synthesized in C. perfringens.

121 ified Agr-like quorum-sensing (QS) system in C. perfringens controls all toxin production by surveyed

122 lture, providing the first evidence that, in C. perfringens, this system can control production of pl

123 est that CPB2 could be an accessory toxin in C. perfringens enterotoxin (CPE)-associated AAD/SD.

124 etic component that explains the variance in C. perfringens strain virulence by assessing patterns of

125 by C. perfringens type A isolates, including C. perfringens type A food poisoning and non-food-borne

126 otentially plasmid-encoded toxins, including C. perfringens enterotoxin and beta2 toxin, encoded by t

127 These results indicate C. perfringens biofilms play an important role in the pe

128 Ingested C. perfringens vegetative cells sporulate in the intesti

129 iocin leucocyclicin Q, capable of inhibiting C. perfringens.

130 rs carrying the fusions were introduced into C. perfringens by electroporation.

131 lucuronidase (gusA) gene and introduced into C. perfringens.

132 al transfer of a nonreplicating plasmid into C. perfringens, which led to inactivation of the ccpA ge

133 is unique for producing the two most lethal C. perfringens toxins, i.e., epsilon-toxin and beta-toxi

134 nsistent with NanI sialidase being the major C. perfringens sialidase when produced, FP and Db strain

135 ases and chromosomal cpe isolates cause most C. perfringens type A food poisoning cases.

136 A dcm gene, which is often present near C. perfringens plasmid-borne toxin genes, was identified

137 suggest that many, if not all, cpe-negative C. perfringens isolates (including type B isolates, whic

138 s were also detected in several cpe-negative C. perfringens isolates carrying plasmids but not in typ

139 when transformed into naturally cpe-negative C. perfringens isolates.

140 8239, were electroporated into cpe-negative C. perfringens type A, B, and C isolates.

141 However, cpb2 genes from nonporcine C. perfringens isolates were not always expressed, at le

142 ium spiroforme culture supernatants, but not C. perfringens types C or D.

143 modules, which are found throughout numerous C. perfringens carbohydrate-active enzymes.

144 DCA), at as low as 50 uM, inhibited 82.8% of C. perfringens growth in Tryptic Soy Broth (P < 0.05).

145 plicate C. perfringens TFP in the ability of C. perfringens to adhere to and move along muscle fibers

146 The ability of C. perfringens to regulate its exosialidase activity, la

147 s may be important factors in the ability of C. perfringens to survive in host tissues when bacterial

148 arning, we identified increased abundance of C. perfringens, as a potential causative agent of GI dis

149 that NanI is important for the adherence of C. perfringens to enterocyte-like cells, NanI sialidase

150 ous investigations into the genetic basis of C. perfringens pathogenicity have focused on toxins and

151 g injection of formalin-fixed whole cells of C. perfringens HN13 (a laboratory strain) and JGS4143 (c

152 omise, and capillary leak characteristics of C. perfringens gas gangrene.

153 widely variable across a large collection of C. perfringens strains.

154 sents the first sequence-based comparison of C. perfringens isolates recovered in clinical cases of P

155 tal events in the mother cell compartment of C. perfringens is not the same as that in B. subtilis an

156 and CPE production in SM101, a derivative of C. perfringens type A food-poisoning strain NCTC8798.

157 Due to the enrichment of C. perfringens in situ, we analyzed frozen duodenal tiss

158 Escape of C. perfringens cells from phagosomes of macrophage-like

159 utation was introduced into the ccpA gene of C. perfringens by conjugational transfer of a nonreplica

160 found to be identical to the CPE0329 gene of C. perfringens strain 13, whose product was labeled as a

161 oxin-encoding genes and the 16S rRNA gene of C. perfringens.

162 s introduced into the pilT and pilC genes of C. perfringens abolished motility and surface localizati

163 e introduced into the sigE and sigK genes of C. perfringens.

164 on-based studies that showed rapid growth of C. perfringens on mucin-based substrates.

165 ctivity in cultures as well as the growth of C. perfringens on sialylated glycans.

166 st to assist epidemiologic investigations of C. perfringens outbreaks.

167 r spores of both C-cpe and P-cpe isolates of C. perfringens and provided evidence that proteins encod

168 A total of 48 isolates of C. perfringens were obtained from different stages of th

169 onents of the spore germination machinery of C. perfringens and several Bacillus species and the bioi

170 PFO was shown to be the primary mediator of C. perfringens-dependent cytotoxicity to macrophages.

171 e developed an oral challenge mouse model of C. perfringens type D enterotoxemia.

172 this study we developed two mouse models of C. perfringens type C-induced lethality.

173 Analyses of a cpb deletion mutant of C. perfringens strain HN13 showed that Cpb is strictly r

174 ens, or isogenic, toxin-deficient mutants of C. perfringens.

175 reference gene set for data normalization of C. perfringens gene expression.

176 XbaI) were evaluated with a select panel of C. perfringens strains.

177 mportant contributors to the pathogenesis of C. perfringens type B infections in domestic animals.

178 l new model for studying the pathogenesis of C. perfringens type D infections.

179 d with the putative reduced pathogenicity of C. perfringens by BEOs contributed to the reduction in g

180 argeting of claudins during pathogenicity of C. perfringens in the gut and a framework for new strate

181 h inducible expression of PilA1 and PilA2 of C. perfringens were constructed.

182 d cpb genes, which indicated the presence of C. perfringens type C.

183 e due to sporulation-dependent production of C. perfringens enterotoxin encoded by the cpe gene.

184 ns exist in Agr-like QS system regulation of C. perfringens toxin production.

185 content is essential for full resistance of C. perfringens spores to moist heat, UV radiation, and c

186 catalytic domains of the three sialidases of C. perfringens and probe their substrate specificity.

187 irst showed that human intestinal strains of C. perfringens can grow by utilizing either glucose or s

188 We have recently shown that strains of C. perfringens move across the surface of agar plates by

189 didate reference genes from three strains of C. perfringens were assessed for stability under various

190 n toxin-producing (ETX-producing) strains of C. perfringens within their gut microbiomes compared wit

191 sis (PFGE) method for molecular subtyping of C. perfringens isolates to aid in epidemiologic investig

192 h PFO and PLC were necessary for survival of C. perfringens in mouse muscle tissue.

193 causes the gastrointestinal (GI) symptoms of C. perfringens type A food poisoning and CPE-associated

194 for causing the gastrointestinal symptoms of C. perfringens type A food poisoning, the second most co

195 D) of SARS-CoV-2, fused to the C-terminus of C. perfringens enterotoxin, which is known to target Cla

196 Fs) known to mediate conjugative transfer of C. perfringens plasmid pCW3.

197 ategies may be possible for the treatment of C. perfringens-mediated myonecrosis.

198 is complex of an inactive (D220N) variant of C. perfringens GH125 enzyme in complex with 1,6-alpha-ma

199 ntial for cortex hydrolysis and viability of C. perfringens spores.

200 However, the viability of C. perfringens spoVA spores was 20-fold lower than the v

201 ts similar cytotoxicity-enhancing effects on C. perfringens enterotoxin and beta toxin, which are als

202 cific NEC cases associated with overabundant C. perfringens termed C. perfringens-associated NEC (CPA

203 sts concerning the association of particular C. perfringens toxinotypes (type A to E) with gastrointe

204 dings suggest both the importance of pfoA(+) C. perfringens as a gut pathogen in preterm infants and

205 ignificant association between CPB2-positive C. perfringens isolates and diarrhea in piglets.

206 notyping and phenotyping of 23 cpb2-positive C. perfringens isolates from horses with GI disease (ref

207 notyping and phenotyping of 29 cpb2-positive C. perfringens isolates from pigs with GI disease (pig G

208 that distinct subpopulations of cpe-positive C. perfringens isolates may be responsible for C. perfri

209 to compare the genotypes of 43 cpe-positive C. perfringens isolates obtained from diverse sources.

210 sion is necessary for these two cpe-positive C. perfringens type A human disease isolates to cause GI

211 factor in GI diseases involving cpe-positive C. perfringens type A isolates.

212 current study by examining 34 cpe-positive, C. perfringens fecal isolates from North American cases

213 us studies showed that NanI could potentiate C. perfringens epsilon toxin cytotoxicity by enhancing t

214 inal defense mechanism against CPB-producing C. perfringens isolates.

215 CPE-producing C. perfringens isolates have also recently been associat

216 r, these findings suggest that ETX-producing C. perfringens strains are biologically plausible pathog

217 C. perfringens type A strains producing C. perfringens enterotoxin (CPE) cause human food poison

218 amples from NEC infants not carrying profuse C. perfringens revealed an overabundance of a Klebsiella

219 e determined and compared with the published C. perfringens strain 13 genome.

220 Interestingly, DCA reduced C. perfringens invasion into ileum (P < 0.05) without al

221 involvement of AbrB repression in regulating C. perfringens sporulation.

222 Based on the RF model and ANCOM results, C. perfringens was identified as a potential causative a

223 biota can be identified in meconium samples; C. perfringens continues to be associated with NEC from

224 s produced only during sporulation and since C. perfringens can sporulate in the intestines.

225 Some C. perfringens isolates also produce the newly discovere

226 CPE is produced by sporulating C. perfringens cells in the small intestinal lumen, wher

227 se was purified from extracts of sporulating C. perfringens cells.

228 Indeed, wild-type and spoVA C. perfringens spores germinated similarly with a mixtur

229 Strikingly, C. perfringens was overrepresented in NMO (p = 5.24 x 10

230 ractical and reproducible means of subtyping C. perfringens libraries from specific epidemiological o

231 ated with overabundant C. perfringens termed C. perfringens-associated NEC (CPA-NEC).

232 Given that C. perfringens alpha-toxin cleaves the phosphocholine he

233 Mechanism studies revealed that C. perfringens induced (P < 0.05) elevated expression of

234 Here we show that C. perfringens produces TFP and moves with an unusual fo

235 We have previously shown that C. perfringens can glide across an agar surface in long

236 These results suggest that C. perfringens type A and C strains that cause human foo

237 Recent studies suggest that C. perfringens type A food poisoning is caused by C. per

238 ecent epidemiological studies suggested that C. perfringens isolates carrying the gene encoding CPB2

239 The C. perfringens cpe gene, encoding CPE, is transcribed fr

240 utralizing monoclonal antibodies against the C. perfringens epsilon-toxin.

241 h as CPA, CPB, and PFO, is controlled by the C. perfringens Agr-like (CpAL) quorum sensing (QS) syste

242 e A isolates carry the cpe gene encoding the C. perfringens enterotoxin.

243 Therefore, C. perfringens mutants lacking PFO and PLC were examined

244 Biotinylated antibodies to C. perfringens alpha toxin bound to streptavidin paramag

245 We evaluated the contribution of ETX to C. perfringens type D pathogenicity in an intraduodenal

246 ded strong synergy to B. fragilis but not to C. perfringens.

247 dynamics of host microbiota in responding to C. perfringens infection.

248 against myonecrotic disease was specific to C. perfringens-mediated myonecrosis; buprenorphine did n

249 Significantly, wild-type C. perfringens cells adhered to mouse myoblasts under an

250 ed on animals infected with either wild-type C. perfringens, or isogenic, toxin-deficient mutants of

251 l in sheep, goats, and mice using a virulent C. perfringens type D wild-type strain (WT), an isogenic

252 s were injected together with killed, washed C. perfringens further substantiated these tissue-destru

253 ates indicated that all of the isolates were C. perfringens alpha-toxin gene positive and 46 of 48 is

254 G+C-content gram-positive bacteria, of which C. perfringens is a member.

255 a chromosomal enterotoxin gene (cpe), while C. perfringens type A isolates responsible for non-food-

256 osomal enterotoxin (cpe) gene (C-cpe), while C. perfringens-associated non-food-borne gastrointestina

257 n of morbidity and mortality associated with C. perfringens gas gangrene.

258 tor responsible for symptoms associated with C. perfringens type A food poisoning, is produced by ent

259 tion chicken experiment, oral challenge with C. perfringens JGS4143 lead to 22% survival, whereas co-

260 diet + 120 mg/kg BEOs), were challenged with C. perfringens from days 14 to 20 and were killed on day

261 mics and functions in chicks challenged with C. perfringens.

262 ity caused by an experimental infection with C. perfringens in a murine model of gas gangrene.