ライフサイエンスコーパス: leukocidin

1 ll as toxic shock toxin and Panton-Valentine leukocidin.

2 shock syndrome toxin 1, and Panton-Valentine leukocidin.

3 mmon toxin genes, including Panton-Valentine leukocidin.

4 ec) typing, and PCR for the Panton-Valentine leukocidin.

5 shock syndrome toxin 1 and Panton-Valentine leukocidin.

6 yard regions as well as the Panton-Valentine leukocidin.

7 d kill leukocytes, known collectively as the leukocidins.

8 essor of cytotoxins, such as alpha-toxin and leukocidins.

9 B and HlgCB as major secreted staphylococcal leukocidins.

10 (DI = 0.566), positive for Panton-Valentine leukocidin (96.3%), and resistant to erythromycin (94.1%

11 Here we demonstrate that leukocidin A/B (LukAB) is required and sufficient for th

12 ement receptor 3, as a cellular receptor for leukocidin A/B (LukAB), an important toxin that contribu

13 In this study, we report that leukocidin A/B (LukAB), the most divergent member of the

14 Among these is LukAB (leukocidin A/leukocidin B), a toxin that assembles into

15 More recently, leukocidin AB (LukAB) has gained interest as a vaccine a

16 Intriguingly, one of the leukocidins, Leukocidin AB (LukAB), is found associated with the bact

17 igericin and the Staphylococcus aureus toxin leukocidin AB (LukAB).

18 peron, which encodes the recently identified leukocidin AB (LukAB).

19 A-MRSA, with an emphasis on Panton-Valentine leukocidin, alpha-hemolysin, and the recently discovered

20 nd translation of genes for Panton-Valentine leukocidin, alpha-hemolysin, and toxic-shock syndrome to

21 uced and prolonged mRNA for Panton-Valentine leukocidin, alpha-toxin, and toxic-shock syndrome toxin

22 , however, in expression of Panton-Valentine leukocidin and in the degree of inflammatory lung damage

23 a number of toxins, such as Panton-Valentine leukocidin and LukAB, that have specificity for human re

24 train with genes coding for Panton-Valentine leukocidin and the arginine catabolic mobile element.

25 A; all carried the gene for Panton-Valentine leukocidin and the gene complex for staphylococcal-casse

26 Although leukocidins and staphylococcal alpha-hemolysin share par

27 an interaction between Staphylococcus aureus leukocidins and their cellular receptor DARC on endothel

28 e vaginal isolate was mecA, Panton-Valentine leukocidin, and staphylococcal enterotoxin B and C negat

29 aureus which encode enterotoxins, exotoxins, leukocidins, and leukotoxins not found in S. epidermidis

30 Bicomponent pore-forming leukocidins are a family of potent toxins secreted by St

31 phylococcus aureus bi-component pore-forming leukocidins are secreted toxins that directly target and

32 alt bridges, not found in other bi-component leukocidins, are essential for dimer formation in soluti

33 Among these is LukAB (leukocidin A/leukocidin B), a toxin that assembles into an octameric

34 L-lipid interaction was sufficient to enable leukocidin complex formation as determined by neutron re

35 receptor interaction enables assembly of the leukocidin complex, targeting of membranes, and insertio

36 Two leukocidins, Leukocidin ED (LukED) and gamma-Hemolysin AB (HlgAB), ar

37 Staphylococcus aureus (SA) leukocidin ED (LukED) belongs to a family of bicomponent

38 Leukocidin ED (LukED) is a pore-forming toxin produced b

39 strains of S. aureus produce toxins such as leukocidins (eg, Panton-Valentine leukocidin, toxic shoc

40 ructure of the oligomeric pore formed by the leukocidin examined here has diverged significantly from

41 ma to lungs made friable by Panton-Valentine leukocidin expressing S. aureus infection.

42 Panton-Valentine leukocidin expressing S. aureus pneumonia can cause seve

43 ients with sputum-confirmed Panton-Valentine leukocidin expressing S. aureus pneumonia managed with e

44 management of patients with Panton-Valentine leukocidin expressing S. aureus pneumonia with extracorp

45 xperience and outcomes with Panton-Valentine Leukocidin expressing S. aureus pneumonia.

46 Panton-Valentine leukocidin expressing Staphylococcus aureus pneumonia, a

47 d 2, and two proteins identified as putative leukocidin F and S subunits of the two-component leukoto

48 reactive between members of the pore-forming leukocidin family.

49 likely to be infected with Panton-Valentine leukocidin gene (pvl)-constitutive MRSA (19% versus 56%;

50 IV, 145 (35.9%) carried the Panton-Valentine leukocidin genes (PVL+), and 162 (40.1%) were identified

51 Cape Verde showed that (i) Panton-Valentine leukocidin genes were present in 35% of the isolates and

52 exotoxin gene profiles (eg, Panton Valentine leukocidin genes) compared with health care-associated i

53 of a staphylococcal pore-forming cytotoxin, leukocidin GH (LukGH), in complex with its receptor (the

54 Until now, six different leukocidins have been described, some of which are host

55 genes which included those for enterotoxins, leukocidins, hemolysins, and surface proteins and severa

56 and cannot produce virulence factors such as leukocidins, hemolysins, or the antioxidant staphyloxant

57 We found that LukMF', a pore-forming leukocidin homolog to the human-specific LukSF-PV toxin,

58 de an unprecedented insight into bicomponent leukocidin-host receptor interaction, enabling the devel

59 Leukocidin-immunized mice produce potent leukocidin-neut

60 Staphylococcus aureus Panton-Valentine leukocidin is a pore-forming toxin targeting the human C

61 lence factors, particularly Panton-Valentine leukocidin, is common in CA-MRSA, emphasizing its potent

62 Intriguingly, one of the leukocidins, Leukocidin AB (LukAB), is found associated

63 Two leukocidins, Leukocidin ED (LukED) and gamma-Hemolysin A

64 Staphylococcal leukocidin (Luk) and alpha-hemolysin (alphaHL) are membe

65 Using the bicomponent pore-forming leukocidin (Luk) exotoxins of the major pathogen Staphyl

66 This is attributed to the leukocidin LukAB, which promotes S. aureus survival duri

67 as the receptor for the S. aureus hemolytic leukocidins LukED and HlgAB.

68 e genes encoding the F and S components of a leukocidin, LukF (HlgB) and LukS (HlgC), a pore-forming

69 identify and characterise a novel S. aureus leukocidin; LukPQ.

70 nst leukotoxin E (LukE) and Panton-Valentine leukocidin (LukS-PV), but not alpha-hemolysin (Hla), wer

71 mponent pore-forming toxins Panton-Valentine leukocidin LukSF-PV (PVL) and gamma-hemolysin CB (HlgCB)

72 her, these results demonstrate that blocking leukocidin-mediated immune evasion can promote host prot

73 We hypothesized that neutralizing leukocidin-mediated immune subversion by vaccination may

74 eremia, we demonstrate that infection with a leukocidin mutant results in increased levels of anti-S.

75 with the WT parental strain, indicating that leukocidins negatively impact the generation of anti-S.

76 Leukocidin-immunized mice produce potent leukocidin-neutralizing antibodies and robust Th1 and Th

77 Neither Panton-Valentine leukocidin nor protein A expression was essential, but i

78 The bi-component leukocidins of Staphylococcus aureus are important virul

79 es tested were positive for Panton-Valentine leukocidin, of which 90% carried staphylococcal chromoso

80 sis (PFGE), spa typing, and Panton-Valentine leukocidin PCR.

81 In addition, the leukocidin pore is weakly cation selective and exhibits

82 Therefore, if the leukocidin pore were a cylinder, its diameter would be a

83 ed arcA and opp3, and 1 was Panton-Valentine leukocidin positive (PVL(+)).

84 solates belonged to the CC8/Panton-Valentine leukocidin-positive (PVL(+)) group of S. aureus clone US

85 e mec (SCCmec) type IV, and Panton-Valentine leukocidin-positive clustered separately from those that

86 d or uncomplicated SAB) and Panton-Valentine leukocidin-positive isolate.

87 of ciprofloxacin-sensitive Panton-Valentine leukocidin-positive methicillin-resistant Staphylococcus

88 Panton-Valentine leukocidin-positive USA300 strains caused 5 of the last

89 vasive infections caused by Panton-Valentine leukocidin-positive, community-associated, methicillin-r

90 Despite the loss of leukocidin production and staphyloxanthin biosynthesis,

91 ysins (HlgAB and HlgCB) and Panton-Valentine leukocidin (PVL or LukSF) were shown to assemble from so

92 ) and isolates positive for Panton-Valentine leukocidin (PVL) (P = 0.008).

93 coccal exotoxins, including Panton-Valentine leukocidin (PVL) and alpha-hemolysin (Hla), although sup

94 Panton-Valentine leukocidin (PVL) and alpha-toxin are exotoxins that crea

95 ed all strains were USA300, Panton-Valentine leukocidin (PVL) and arginine catabolic mobile element (

96 pa) typing and detection of Panton-Valentine leukocidin (PVL) and scn genes.

97 s aureus strains expressing Panton-Valentine leukocidin (PVL) are associated with severe skin and sof

98 ureus (MRSA) expressing the Panton-Valentine leukocidin (PVL) are rampant, but the contribution of PV

99 nent CA-MRSA strain encodes Panton-Valentine leukocidin (PVL) cytotoxin genes, belongs to pulsed fiel

100 some mec (SCCmec) types and Panton-Valentine leukocidin (PVL) gene carriage were compared among suspe

101 The lukF/lukS Panton-Valentine leukocidin (PVL) genes did not directly correlate with t

102 microdilution, detection of Panton-Valentine leukocidin (PVL) genes, arginine catabolic mobile elemen

103 , as well as assays for the Panton-Valentine leukocidin (PVL) genes, the protein A gene (spa), and ar

104 sition of the phage-encoded Panton-Valentine leukocidin (PVL) genes.

105 ted for the presence of the Panton-Valentine leukocidin (PVL) genes.

106 sociated with SCCmec IV and Panton-Valentine leukocidin (PVL) genes.

107 The role of the Panton Valentine leukocidin (PVL) in CA-MRSA pathogenesis is a matter of

108 The role of Panton-Valentine leukocidin (PVL) in determining the severity and outcome

109 The role of Panton-Valentine leukocidin (PVL) in Staphylococcus aureus infections is

110 sThe role of Panton-Valentine leukocidin (PVL) in Staphylococcus aureus pathogenesis i

111 The Panton-Valentine leukocidin (PVL) is a cytotoxin expressed by many methic

112 have hypothesized that the Panton-Valentine leukocidin (PVL) is a key virulence determinant in CA-MR

113 Panton-Valentine leukocidin (PVL) is a pore-forming toxin secreted by Sta

114 The Staphylococcus aureus Panton-Valentine leukocidin (PVL) is a pore-forming toxin secreted by str

115 Panton-Valentine leukocidin (PVL) is a two-component cytolytic toxin epid

116 Panton-Valentine leukocidin (PVL) is common in African Staphylococcus aur

117 The S. aureus toxin Panton-Valentine leukocidin (PVL) is most likely causative for necrotizin

118 or a bacteriophage encoding Panton-Valentine leukocidin (PVL) lysogenized into its chromosome (propha

119 al susceptibility patterns, Panton-Valentine leukocidin (PVL) occurrence, and staphylococcal cassette

120 The Panton-Valentine leukocidin (PVL) of Staphylococcus aureus can be associa

121 The impact of Panton-Valentine leukocidin (PVL) on the outcome in Staphylococcus aureus

122 mec type IV, and 61.5% were Panton Valentine leukocidin (PVL) positive.

123 Panton-Valentine leukocidin (PVL) production by methicillin-resistant Sta

124 l strains were subjected to Panton-Valentine leukocidin (PVL) screening, and SCCmec, pulsed-field gel

125 USA300 secretes Panton-Valentine leukocidin (PVL) toxin, which is associated with highly

126 Panton-Valentine leukocidin (PVL) was present in 21.9%, and vancomycin he

127 PV and lukF-PV encoding the Panton-Valentine leukocidin (PVL) were present in all CAMRSA SSTI isolate

128 Panton-Valentine leukocidin (PVL), a bacteriophage encoded toxin that has

129 Panton-Valentine leukocidin (PVL), a pore-forming cytotoxin, has garnered

130 CA-MRSA strains, expresses Panton-Valentine leukocidin (PVL), a pore-forming toxin that targets poly

131 were compared with those of Panton-Valentine leukocidin (PVL), a well-characterized S. aureus leukoto

132 detection of genes encoding Panton-Valentine leukocidin (PVL), and antimicrobial resistance determina

133 olic mobile element (ACME), Panton-Valentine leukocidin (PVL), and other toxins that may contribute t

134 )mec type IV, the genes for Panton-Valentine leukocidin (PVL), and the enterotoxin Q and K genes.

135 STI CA-MRSA strains produce Panton-Valentine leukocidin (PVL), but its contribution to CA-MRSA pathog

136 whether a virulence factor, Panton-Valentine leukocidin (PVL), could account for the high rates of MR

137 Panton-Valentine leukocidin (PVL), encoded by the lukSF-PV genes, is a pu

138 A single toxin, Panton-Valentine leukocidin (PVL), has been linked by epidemiological stu

139 virulence factors, such as Panton-Valentine leukocidin (PVL), have been proposed to drive this epide

140 cytolytic toxins, including Panton-Valentine leukocidin (PVL), leukotoxin GH (LukGH; also known as Lu

141 [SCCmecIV]) and carried the Panton-Valentine leukocidin (pvl), lukD, and lukE genes, but no other tox

142 the USA300 characteristics Panton-Valentine leukocidin (PVL), SCCmec IVa, the arginine catabolic mob

143 la), delta-hemolysin (Hld), Panton Valentine leukocidin (PVL), staphylococcal enterotoxin C-1 (SEC-1)

144 phoresis (PFGE) and PCR for Panton-Valentine leukocidin (PVL), the arginine catabolic mobile element

145 mecA and mupA and those for Panton-Valentine leukocidin (PVL), USA300, and USA400.

146 gene, encoding part of the Panton-Valentine leukocidin (PVL), was observed in the codY mutant.

147 y alpha-hemolysin (Hla) and Panton-Valentine leukocidin (PVL), we evaluated whether active immunizati

148 MRSA LAC(WT) USA300 and its Panton-Valentine leukocidin (PVL)- and alpha-hemolysin (Hla)-negative iso

149 esistance, SCCmec type, and Panton-Valentine leukocidin (PVL)-producing genes on an S. aureus genome.

150 arA, alpha-toxin (hla), and Panton-Valentine leukocidin (pvl).

151 es for the virulence factor Panton-Valentine leukocidin (PVL).

152 in, secreted proteases, and Panton-Valentine leukocidin (PVL).

153 ns harboring genes encoding Panton-Valentine leukocidin (PVL).

154 , alpha-hemolysin (Hla) and Panton-Valentine leukocidin (PVL; LukF-PV/LukS-PV subunits), both premier

155 ype, toxin genes (e.g., for Panton-Valentine leukocidin [PVL]), and staphylococcal cassette chromosom

156 is, but the closely related Panton-Valentine leukocidin S (LukS-PV) does not bind to DARC and is not

157 hereby challenging the current paradigm that leukocidin specificity is driven solely by the S-compone

158 romosome mec (SCCmec) type, Panton-Valentine leukocidin status, and multilocus sequence type.

159 We observed that, unlike other leukocidin subunits, recombinant LukH and LukG had low s

160 host cells and provide key insights into how leukocidins target membranes.

161 to depend on the production of pore-forming leukocidins that kill leukocytes and lyse erythrocytes.

162 The contribution of these leukocidins to impair the development of anti-S. aureus

163 The potential for S. aureus leukocidins to manipulate vascular integrity highlights

164 f pore-forming toxins, known as bi-component leukocidins, to evade the host immune response and promo

165 ns such as leukocidins (eg, Panton-Valentine leukocidin, toxic shock syndrome toxin 1, exfoliative to

166 well as for the design of drugs antagonizing leukocidin toxicity.

167 to detect mecA, mecC, vanA, Panton-Valentine Leukocidin toxin (PVL), and toxic shock syndrome toxin-1

168 SCCmec type IV and the Panton-Valentine leukocidin toxin gene were detected in 98 percent of MRS

169 lates were positive for the Panton-Valentine leukocidin toxin genes and agr I.

170 assette chromosome mec, and Panton-Valentine leukocidin typing.

171 ns SpA and Sbi, and neutralizes pore-forming leukocidins via fusion with anti-toxin centyrins, while

172 ed 4 h after infection, and Panton-Valentine leukocidin was maximally expressed 72 h after infection,

173 The bicomponent toxin Panton-Valentine leukocidin was not produced during intracellular infecti

174 e pore-forming properties of the recombinant leukocidin were also investigated with planar lipid bila

175 secreted toxins, including Panton-Valentine leukocidin, were highly expressed during superficial and

176 riage of the genes encoding Panton-Valentine leukocidin, while common among MRSA of PFGE type USA300,

177 data support epidemiological studies linking leukocidins with human SSTIs and highlight the power of