ライフサイエンスコーパス: meningococci

1 ine against infections caused by serogroup B meningococci.

2 ent of a mucosal vaccine against serogroup B meningococci.

3 charide vaccines protect against serogroup C meningococci.

4 fter immunization with homologous whole-cell meningococci.

5 f the role of active immune response against meningococci.

6 r cells that had been exposed to heat-killed meningococci.

7 of healthy donors are exposed to heat-killed meningococci.

8 eripheral blood mononuclear cells exposed to meningococci.

9 eripheral blood mononuclear cells exposed to meningococci.

10 rvoirs for all of the exl cassettes found in meningococci.

11 from all 12 macaques enhanced FH binding to meningococci.

12 ingioma cell that was not apparent with Cap+ meningococci.

13 osed of polysaccharides from pneumococci and meningococci.

14 confirmed by [3H]-palmitic acid labelling of meningococci.

15 es, we show that these receptors are used by meningococci.

16 sepsis and meningitis caused by serogroup B meningococci.

17 confidence interval [CI], 3.2%-3.6%) carried meningococci.

18 d with sepsis and recoverable levels of live Meningococci.

19 on results from reduced carriage of virulent meningococci.

20 required for complement-dependent killing of meningococci.

21 act on immune escape and host persistence of meningococci.

22 ng, we identified five distinct GGI types in meningococci.

23 their bactericidal activity against group B meningococci.

24 at demonstrated human-specific fH binding to meningococci.

25 ains fH SCR 6, also bound to fHbp-expressing meningococci.

26 majority of disease-associated group B and C meningococci.

27 antly upregulated in blood after exposure to meningococci.

28 gococci, but not the CPS of serogroup B or C meningococci.

29 o the development of immunity to serogroup B meningococci.

30 ein-labeled ligands to HpuAB on live, intact meningococci.

31 urified PorB inhibited the binding of MBL to meningococci.

32 four of the five major pathogenic groups of meningococci: A, C, W-135, and Y.

33 e purified human LOS-specific IgG that binds meningococci across LOS glycose-specific serotypes.

34 meningococci that (rate ratio, 0.06); these meningococci also exhibited high rates of capsule expres

35 We determined that meningococci also release PG fragments during growth, in

36 o explain the preponderance of 3-PEA-bearing meningococci among clinical isolates, because 6-PEA enha

37 permeability-increasing protein, which kills meningococci and binds to and clears bacterial endotoxin

38 OMVs from both meningococci and commensal neisseriae have shown promise

39 SBA titres most likely reflects exposure to meningococci and consecutive reactive immunity.

40 ents indicated that AutB is not expressed in meningococci and does not cross-react with AutA.

41 -expressing clinical and mucosal isolates of meningococci and gonococci were shown to bind to the CD6

42 g may be an important virulence mechanism of meningococci and other encapsulated bacterial pathogens.

43 oduce vaccines with broad protection against meningococci and pneumococcus, develop an effective vacc

44 surface of wild-type but not Deltamip mutant meningococci and showed bactericidal activity against ho

45 specificity of the bactericidal response to meningococci and the stability of expression of the clas

46 ca, was due both to displacement of existing meningococci and to inhibition of new acquisition, and p

47 bster mice were inoculated intranasally with meningococci, and bacteria were recovered from the noses

48 Escherichia coli K1, groups W-135, Y, and C meningococci, and group B Streptococcus capsular polysac

49 All meningococci are carried in the nasopharynx, and most ge

50 Serum bactericidal assays (SBAs) for Group B meningococci are considered the methods of choice for th

51 Individual strains of meningococci are extremely variable and undergo dynamic

52 Meningococci are opportunistic pathogens that colonize t

53 n transglycosylase, elicits protective Ab to meningococci as a result of mimicking an epitope on loop

54 Carriage of meningococci, as detected by the combined methods, was 2

55 Meningococci bind fH via fH binding protein (fHbp), a su

56 acetylated the wild-type CPS of serogroup A meningococci, but not the CPS of serogroup B or C mening

57 We conclude that MBL binds to meningococci by a novel target recognition of two nongly

58 mon resonance and to the mutant expressed on meningococci by flow cytometry.

59 ect individuals can block killing of group B meningococci by human sera that are otherwise bactericid

60 There was no evidence of internalization of meningococci by meningioma cells in vitro, an observatio

61 Disk diffusion testing with meningococci can be performed in a reproducible manner w

62 We conclude that group C meningococci can be phagocytosed by neutrophils in the a

63 Meningococci can escape being killed by antibodies to LP

64 n analysis of the hemA mutant indicated that meningococci can transport intact porphyrin from heme (H

65 termine the evolutionary relationships among meningococci carrying hmbR, exl2, or exl3, isolates repr

66 d Kingdom in 1999, but the sequence types of meningococci causing disease since that time have not ye

67 In contrast, meningococci contain at least one L-LDH in addition to t

68 The detection of carriage of serogroup B meningococci correlated with an increase in detection of

69 ntains a poly(G) tract, which suggested that meningococci could phase vary each Hb receptor independe

70 by clonal complex ST-11 and ST-8 serogroup C meningococci decreased from 251 of 268 (94%) before, to

71 Little is known about how meningococci directly influence these receptors.

72 On occasion, meningococci disseminate from the nasopharynx to cause i

73 Meningococci drive the differentiation of the Men C-spec

74 Encapsulated meningococci expressing a Hep2(GlcNAc)-->KDO2-->lipid A

75 y herd protection by reduced colonization of meningococci expressing the MenC capsule.

76 st strains representative of disease-causing meningococci expressing vaccine-heterologous antigens.

77 st strains representative of disease-causing meningococci expressing vaccine-heterologous antigens.

78 Some strains of meningococci form biofilms, and this process is likely i

79 d multilocus sequence typing to characterize meningococci from patients with invasive disease over a

80 n vitro data suggest that, in these lesions, meningococci gain access from the capillary lumen to the

81 l be safe and effective vaccines for Group B meningococci (GBMs), Escherichia coli K1, and Pasteurell

82 These enzymes are active in meningococci grown in complex media and are not dependen

83 For meningococci grown on a complex medium, activity of the

84 , E (3 isolates), and X (2 isolates), and 68 meningococci had the capsule-null intergenic region.

85 MenAfriVac (PsA-TT), disease due to group A meningococci has nearly disappeared.

86 Pathogenic meningococci have acquired a 24 kb capsule synthesis isl

87 rane protein (OMP) components of serogroup B meningococci have been shown to be effective in clinical

88 Thus, App is conserved among meningococci, immunogenic in humans and potentially invo

89 Carriage of all strains of serogroup C meningococci in asymptomatic students was low (0.9%), an

90 dy shows high seroprevalence against group A meningococci in Burkina Faso following MenAfriVac introd

91 ereas endotoxin was at least as effective as meningococci in inducing ICAM-1 and VCAM-1.

92 We compared the carriage of meningococci in isolates we obtained from 14,064 student

93 asis for LOS sialylation in AP regulation on meningococci in more than one animal species.

94 Killing of meningococci in reactions containing bactericidal mAbs a

95 ide (LOS) are bactericidal for L3,7 and L2,4 meningococci in the presence of human complement.

96 duction of oropharyngeal carriage of group A meningococci in vaccinated and unvaccinated individuals,

97 rnatants of inflammatory cells stimulated by meningococci in vitro abolished the negative inotropic a

98 Meningococci incubated with human serum bound MBL as det

99 ty and morbidity associated with serogroup B meningococci infections, but uncertainty remains about t

100 situation with gonococci, the mtr system in meningococci is not subject to the MtrR or MtrA regulato

101 We conclude that the mtr efflux system in meningococci is subject to transcriptional regulation by

102 Six clusters contained carried meningococci isolated during 1997-2001, suggesting tempo

103 repertoires in 190 asymptomatically carried meningococci isolated in the United Kingdom from a conte

104 Opa repertoires in 227 disease-associated meningococci, isolated in the United Kingdom over a peri

105 The lack of meningococci killing by blood containing eculizumab resu

106 Over the past 50 years one such lineage of meningococci, known as serogroup A, clonal complex 5 (A:

107 The ability of meningococci lacking expression of fHbp and NspA to caus

108 is aggregated and recruited to intracellular meningococci (MC).

109 An equivalent vaccine against group B meningococci (menB) has remained elusive due to the poor

110 Following challenge with meningococci, meningioma cells secreted specifically the

111 As for meningococci, mutation of the gonococcal lldA reduced L-

112 The transcriptome of adherent meningococci obtained after 4 h of coculture was markedl

113 Meningococci obtained from cerebrospinal fluid or oropha

114 Understanding why carriers of meningococci occasionally develop invasive disease is a

115 enicity and cross-reactivity of AutA amongst meningococci of different serogroups and strains represe

116 us-mediated adhesion to host cells by either meningococci or gonococci triggers the rapid, localized

117 rmine whether carried and disease-associated meningococci possess different Opa repertoires and wheth

118 Meningococci possessing a capsule null locus (cnl) typic

119 ely formed amide linkages, whereas C4B bound meningococci preferentially via ester linkages.

120 meningitidis and N. gonorrhoeae showed that meningococci release less of the proinflammatory PG mono

121 No studies have determined if meningococci release PG or activate Nod1 during infectio

122 ngitis and septicaemia caused by serogroup B meningococci remain uncontrolled.

123 t, efficient stimulation of RANTES by intact meningococci required pilus-mediated adherence, which se

124 To ascertain the mechanisms by which meningococci resist PxB, mutants that displayed increase

125 Purified CPSs bound to unencapsulated meningococci, simulated findings with naturally encapsul

126 might induce against the diverse serogroup B meningococci strains that cause disease.

127 However, different strains of meningococci, such as those within the electrophoretic t

128 thelial cells were invaded by Opa-expressing meningococci, suggesting that epithelial cell invasion m

129 any years in other, unrelated, hyperinvasive meningococci, suggesting that the epidemic clones emerge

130 of sequence type (ST)-11 complex serogroup C meningococci that (rate ratio, 0.06); these meningococci

131 The presence of cnl meningococci that can escape serum killing and cause inv

132 expression did not alter factor H binding to meningococci that express gonococcal Por.

133 hat MCC vaccines protect against carriage of meningococci that express serogroup C polysaccharide cap

134 pa protein increased the association of Cap+ meningococci that expressed low-adhesive pili, but did n

135 re found to be constitutively transcribed in meningococci, the biosynthesis operon about fourfold hig

136 growing evidence for RNA-based regulation in meningococci, their transcriptome structure and output o

137 In meningococci, three different TPS systems exist, and of

138 proteins mediated by phase variation enable meningococci to escape killing in vitro by bactericidal

139 c mutant strains of groups A, B, C, W, and Y meningococci to express similar amounts of the same fact

140 ein that is required for optimal adhesion of meningococci to human cells.

141 in an increased resistance of gonococci and meningococci to the same compounds, as well as to norflo

142 Factor H binding to unsialylated meningococci transfected with gonococcal Por1B was simil

143 y altered in a TonB- mutant and in wild-type meningococci treated with the protonophore carbonylcyani

144 Taken together, these data indicated that meningococci utilize multiple mechanisms including the a

145 he IS1106 element downstream of porA in some meningococci was absent in the gonococcus.

146 ine on the prevalence of carriage of group C meningococci was consistent with herd immunity.

147 Immunity to meningococci was determined in infected and uninfected s

148 was restored when binding of blocking Ab to meningococci was inhibited using either synthetic peptid

149 his intervention on asymptomatic carriage of meningococci was investigated to establish whether serog

150 Carriage of serogroup C meningococci was reduced by 66% (p=0.004).

151 e molecules in AP regulation in encapsulated meningococci was studied using isogenic mutants.

152 acid, the capsular polysaccharide of Group B meningococci, we have investigated its solution dynamics

153 Meningococci were added to anticoagulated blood from 12

154 viduals colonized long term with serogroup B meningococci were also upregulated during prolonged cocu

155 Once internalized, meningococci were effectively killed, although more rapi

156 immediately cultured on selective media, and meningococci were identified and serologically character

157 n a total of 48,309 samples, from which 8599 meningococci were isolated and characterized by genotypi

158 Meningococci were isolated from oropharyngeal swabs coll

159 Meningococci were more potent stimuli of CD62E expressio

160 Meningococci were recovered from the animals by nasophar

161 of 25 other genetically diverse nongroupable meningococci were studied in detail.

162 dal and opsonophagocytic for P1.7-expressing meningococci, whereas human MAb SS269 (IgG3) and murine

163 the interactions of piliated and nonpiliated meningococci, whereas lipopolysaccharide (LPS) had a min

164 Opc did not influence the adherence of Cap+ meningococci, whereas loss of capsule was associated wit

165 sis factor-alpha by monocytes in response to meningococci, whereas lower concentrations enhanced the

166 n about classical pathway (CP) inhibition by meningococci, which forms the basis of this study.

167 ms, including encapsulated serogroup B and C meningococci, which leads to increased bacterial killing

168 However, meningococcal lipid A, expressed by meningococci with defects in 3-deoxy-D-manno-octulosonic

169 lic acid capsule modifies the interaction of meningococci with human macrophages at multiple steps, i

170 MBL increased the association of killed meningococci with neutrophils, monocytes, and macrophage

171 Interaction of meningococci with nonhuman complement is relevant for an