ライフサイエンスコーパス: pneumococci

1 e and 50 specimens were culture positive for pneumococci).

2 fection favors nasopharyngeal acquisition of pneumococci.

3 th RSV for 72 hours and then challenged with pneumococci.

4 ctin to purified PspC and to PspC-expressing pneumococci.

5 uptake were impaired by elevated c-di-AMP in pneumococci.

6 purified C1q to various clinical isolates of pneumococci.

7 h before to 2 h after the administration of pneumococci.

8 asal infection of mice with serotype 4 or 6A pneumococci.

9 high rates of nasopharyngeal acquisition of pneumococci.

10 nventional de novo biosynthesis of serine by pneumococci.

11 e, Gram stain, or urinary Binax demonstrated pneumococci.

12 ecting for the outgrowth of CRISPR-defective pneumococci.

13 essential for the transformation process in pneumococci.

14 trated that human, but not mouse, C4BP bound pneumococci.

15 2 isolates previously labeled as nontypeable pneumococci.

16 bind to phosphocholine, C-polysaccharide, or pneumococci.

17 splay higher antibody concentrations against pneumococci.

18 expression induced by lipoteichoic acid and pneumococci.

19 d not the intact apolactoferrin, which kills pneumococci.

20 tself rapidly clear small initial numbers of pneumococci.

21 dynamics and improved interventions against pneumococci.

22 by a serine protease in order for it to kill pneumococci.

23 mulating the killing of complement-opsonized pneumococci.

24 unknown - role in protein phosphorylation in pneumococci.

25 the upper airway lumen, where they engulfed pneumococci.

26 6A, 6B, 6C, and 19A but did not opsonize 19F pneumococci.

27 mage in mice receiving serotypes 2, 3, and 4 pneumococci.

28 atory circuits for lung-specific invasion by pneumococci.

29 first line of defense against invading lung pneumococci.

30 icillin-resistant and erythromycin-resistant pneumococci.

31 mice infected with wild-type PcpA-expressing pneumococci.

32 A total of six (3.4%) patients carried pneumococci.

33 (GyrA G79A) identified here in CL-resistant pneumococci.

34 compared to the clearance of nonencapsulated pneumococci.

35 r FH deposition to the surface of the intact pneumococci.

36 occi or supernatant from overnight growth of pneumococci.

37 l and a pneumonia model with capsular type 3 pneumococci.

38 nical problems or insufficient growth of the pneumococci.

39 ajor epidemic clones of penicillin-resistant pneumococci.

40 the efficacy of opsonophagocytic killing of pneumococci.

41 nate asymptomatic carriage with vaccine-type pneumococci.

42 ntibodies mediate the killing of serotype 6E pneumococci.

43 scribed approximately 90% of the serotype 6E pneumococci.

44 s were able to elicit killing of serotype 6E pneumococci.

45 in vitro mediator production to heat-killed pneumococci.

46 for both meningitis- and bacteremia-causing pneumococci.

47 he activation of purified human platelets by pneumococci.

48 nasopharyngeal carriage of vaccine-serotype pneumococci.

49 that have not been described in encapsulated pneumococci.

50 umbers, is crucial for prolonged carriage of pneumococci.

51 actor predicting antimicrobial resistance in pneumococci.

52 gene was highly conserved within the typical pneumococci (0.3% nucleotide divergence), but was also p

53 iaA gene was found to be specific to typical pneumococci, 100% conserved, and absent from the oral st

54 ct against 62.9% of all circulating invasive pneumococci (78.3% in under-5-year-olds).

55 olates including several capsule serotype 14 pneumococci, a dominant serotype among disease isolates.

56 and their clonal associations is critical as pneumococci adapt to the selective pressures exerted by

57 Systemic challenge with virulent serotype 3 pneumococci also induced anti-dsDNA IgA production in im

58 Dispersed pneumococci also upregulated genes associated with produ

59 These findings demonstrate how pneumococci alter their CPS structure and their immunolo

60 mation in humans on mucosal immunity against pneumococci and a lack of suitable adjuvants for new vac

61 xB, which induces an apoptosis-like death in pneumococci and confers a selective advantage in nasopha

62 reduces the recruitment of soluble hTSP-1 by pneumococci and decreases hTSP-1-mediated pneumococcal a

63 PCR-based methods enhanced the isolation of pneumococci and detection of serotype diversity, with th

64 ed useful in distinguishing between atypical pneumococci and other streptococcal species.

65 rBPI21 bound to pneumococci and pneumolysin (Ply) in a direct and specif

66 nsforming principle (TP) to be purified from pneumococci and prions from scrapie-infected hamster bra

67 tions in the normal human host were toxic to pneumococci and that bacterial survival in vivo depended

68 kappaB activation is a virulence property of pneumococci and that the appropriate activation of macro

69 ergence), but was also present in "atypical" pneumococci and the closely related species S. mitis and

70 t protein C1q, as a molecular bridge between pneumococci and the host, which promotes bacterial cellu

71 lso able to increase the immune adherence of pneumococci and their transfer to macrophages.

72 and conjugative elements in the evolution of pneumococci and, more particularly, the emergence of the

73 respiratory viral infections, acquisition of pneumococci, and development of disease in humans needs

74 eumoniae, trends in the serotype of invasive pneumococci, and invasive pneumococci antimicrobial resi

75 yzed the genetic diversity among serogroup 6 pneumococci, and investigated whether pneumococcal conju

76 nt, microscopic lesions that are filled with pneumococci; and (3) the bacterial virulence determinant

77 rotype of invasive pneumococci, and invasive pneumococci antimicrobial resistance patterns, in India.

78 In the bloodstream, a small percentage of pneumococci appeared as piliated, RrgA-expressing, DivIV

79 oline residues to the virulence potential of pneumococci appears to be the role that these amino alco

80 Within the serotypes, serogroup 6 pneumococci are a frequent cause of serious disease and

81 studies have indicated that biofilm-derived pneumococci are avirulent.

82 nstrate in a mouse model that NanA-deficient pneumococci are impaired in their ability to cause both

83 ly, we observed that if complement-opsonized pneumococci are injected intravenously with CR1(+) mouse

84 Using biophotonic imaging, we observed that pneumococci are rapidly trapped in the spleens of L. don

85 derable competency for genetic exchange, all pneumococci are under considerable pressure to retain ke

86 d cohort studies have questioned the role of pneumococci as the most frequent pathogen causing severe

87 Mothers acquired pneumococci at lower rates (per 1,000 days) from unmeasu

88 orating Centre for Reference and Research on Pneumococci at the Statens Serum Institute (SSI) in Cope

89 In the presence of antibody and complement, pneumococci attach to erythrocytes in a process called i

90 neumococci to erythrocytes in vitro, and the pneumococci attached to erythrocytes via CR1 can be tran

91 so found that the absence of LDH renders the pneumococci avirulent after intravenous infection and le

92 ociated with adult carriage of PCV7-serotype pneumococci before and after the introduction of PCV7 in

93 Thus, pneumococci bind complement inhibitors such as C4b-bindi

94 I21 following intranasal inoculation of Ply+ pneumococci both enhanced upper respiratory tract cell a

95 which we used 25 mug of CRP and 10(7) CFU of pneumococci, both wild-type and mutant CRP protected mic

96 ontypeable due to autoagglutination but were pneumococci by all tests and represented pneumococcal se

97 Thus, the killing of pneumococci by apolactoferrin appears to require a prote

98 oth psaA and ply positive and clustered with pneumococci by MLST (2 were bile soluble); 8 lacked psaA

99 gs challenge whether all clinically relevant pneumococci can be definitively categorized into distinc

100 Transparent-phase pneumococci can be readily washed from the outer surface

101 Previously, we showed that pneumococci can gain access to the CNS through a nonhema

102 the use of the ply gene for the detection of pneumococci can lead to false-positive reactions in the

103 We also demonstrate that pneumococci can utilize the hyaluronic acid capsule of o

104 Pneumococci cause meningitis by invading the blood and p

105 Wild-type pneumococci caused disruption to the ependyma, but this

106 CSF infection of rats with wild-type pneumococci caused meningitis within 26 h, whereas isoge

107 Serotype 11A pneumococci characteristically express capsule beta-gala

108 Analyzing pneumococci collected from children in Massachusetts, we

109 us sequence typing to samples of 126 and 222 pneumococci collected in 2001 and 2004, respectively, fr

110 of pneumococcal meningitis, we observe that pneumococci colocalize with the two BBB endothelial rece

111 hanced clearance of Deltaply PspA(-) PspC(-) pneumococci compared to the clearance of nonencapsulated

112 explain why nearly all clinical isolates of pneumococci conserve this enzyme despite the lethal sele

113 Pneumococci could evade pneumococcal conjugate vaccines

114 It has long been known that about 60% of pneumococci could utilize the fructooligosaccharide inul

115 and multilocus sequence typing data for 426 pneumococci dated from 1937 through 2007 were analyzed.

116 g incubation with RSV or purified G protein, pneumococci demonstrated a significant increase in the i

117 lated to each other and different from other pneumococci despite similar genetic content.

118 Seven percent (52 of 749) had pneumococci detected in blood.

119 icasone plus AC before infection with viable pneumococci developed significantly more lung CFUs at 48

120 Addition of HAMLET to pneumococci dissipated membrane polarity, but depolariza

121 As pneumococci do not produce catalase or an inducible regu

122 rotein A (PspA), a major virulence factor of pneumococci, effectively inhibits C3 deposition.

123 Pneumococci engage vitronectin, the human adhesive glyco

124 ed that coinfection with influenza virus and pneumococci enhanced both colonization and inflammatory

125 lecule, also binds to PC, and CRP binding to pneumococci enhances complement C3 deposition through th

126 n grown in human nasal airway surface fluid, pneumococci exhibited both short- and long-chain forms.

127 lactate production confirmed that dispersed pneumococci exhibited increased metabolism compared to t

128 e disease, which may suggest that colonizing pneumococci exist in biofilm communities that are more r

129 What is more, pneumococci existed as intravacuolar bacteria or escaped

130 As pneumococci express a hyaluronate lyase (Hyl) that cleav

131 Thus, pneumococci express a versatile repertoire of surface pr

132 t allow for efficient colonization, virulent pneumococci express capsules that confer resistance to o

133 Also, Dob1 could opsonize pneumococci expressing serotypes 6A, 6B, 6C, and 19A but

134 plement deposition and phagocytic killing of pneumococci expressing ST11A but not those expressing ST

135 riants were more likely to be colonized with pneumococci expressing those variants.

136 Overall, isolation of pneumococci followed by MP-PCR quickly and accurately id

137 On the basis of these data, we conclude that pneumococci form biofilms in vivo and that this process

138 In this study, we analyzed whether pneumococci form biofilms in vivo, and if so, whether bi

139 Here, we show for the first time that pneumococci form highly structured biofilm communities d

140 disease caused by antibiotic-nonsusceptible pneumococci from 1996 through 2004.

141 za A virus (IAV) infection releases virulent pneumococci from biofilms in vitro and in vivo.

142 approach to distinguish genuine nontypeable pneumococci from closely related nontypeable streptococc

143 how PspA and PspC act in synergy to protect pneumococci from complement-dependent clearance during i

144 his adherence and the subsequent transfer of pneumococci from erythrocytes to macrophages are both de

145 human erythrocytes and improved transfer of pneumococci from erythrocytes to phagocytes.

146 cal isolates in a data set of 121 untypeable pneumococci from nasopharyngeal swabs and middle ear flu

147 has been proposed to electrostatically repel pneumococci from phagocytic cells, and avoidance of phag

148 Clearance of pneumococci from the alveolar space in LPL(-/-) mice was

149 as been shown to allow improved clearance of pneumococci from the blood of mice and to decrease pneum

150 ortant effector cells delaying the spread of pneumococci from the brain to the systemic circulation a

151 correlated with enhanced early clearance of pneumococci from the lung, decreased bacterial invasion

152 epidemiologically with the dissemination of pneumococci from the nasopharynx to the middle ear.

153 prolonged carriage and leads to clearance of pneumococci from the nasopharynx.

154 er of tandem repeat analyses clustered these pneumococci from the other serotype 5 pneumococci in the

155 in PspC expression during the transition of pneumococci from the peritoneum to the blood.

156 presumably through decreased transmission of pneumococci from vaccinated children to adults.

157 CbpG on the surface of pneumococci (full length) or released into the supernata

158 cular Microbiology, Rued et al. show that in pneumococci GpsB forms complexes with PBP2a and PBP2b, a

159 Pneumococci grown anaerobically or genetically lacking p

160 Pneumococci harboring these genes show increased growth

161 on involves opacity phase variation, whereby pneumococci harvested from the nasopharynx are typically

162 zation in mice by exposure to live or killed pneumococci has been shown to be antibody independent bu

163 Pneumococci have evolved several strategies to circumven

164 Pneumococci have evolved several strategies to evade the

165 he CSF were similar after infection with all pneumococci; however, neutrophils and monocytes predomin

166 ngs infected with wild type and DeltapotABCD pneumococci identified expression of proteins that could

167 f mixed killed bacterial vaccines containing pneumococci identified significant heterogeneity among s

168 Adults were more likely to carry PCV7-type pneumococci if they lived with a child <5 years old or i

169 a vital role in opsonophagocytic killing of pneumococci in blood.

170 d intravenous challenge with capsular type 3 pneumococci in CBA/N mice.

171 at least 53% of pneumonia cases were due to pneumococci in HIV-infected South African adults.

172 d reduced mortality, diminished outgrowth of pneumococci in lungs, and reduced dissemination of the i

173 Strikingly, CAT-expressing pneumococci in mouse lungs were outcompeted by susceptib

174 e peritoneum can influence PspC expressed by pneumococci in the blood.

175 stance over a quarter century among invasive pneumococci in the Cleveland area, as well as the reduct

176 Wild-type infections resulted in pneumococci in the CSF and cortical homogenates, but a m

177 show enhanced biofilm formation in vitro by pneumococci in the presence of H. influenzae.

178 these pneumococci from the other serotype 5 pneumococci in the United Kingdom, highlighting the impo

179 This access is thought to occur when the pneumococci in the upper sinus follow the olfactory nerv

180 proapoptotic activity of Ply+ (but not Ply-) pneumococci in TLR4-defective murine macrophages (known

181 yngeal carriage of Streptococcus pneumoniae (pneumococci) in nine Alaskan communities and used an alg

182 Immunization with pneumococci increased anti-oxLDL IgM levels and led to a

183 ability of these immune cells to phagocytose pneumococci independent of capsule.

184 SpnD39III is ubiquitous in pneumococci, indicating an essential role in its biology

185 We show that serotype 2 or 4 pneumococci induce only modest levels of CXCL8 expressio

186 46a as one putatively important regulator of pneumococci-induced host cell activation.

187 The pneumococci-induced oxidative stress was independent of

188 cells, following 4 h of exposure of cells to pneumococci infection.

189 transformation of nonencapsulated, avirulent pneumococci into capsulated, virulent strains during inf

190 own that the intravenous (i.v.) injection of pneumococci into CR1(+) mice also results in more rapid

191 at enhances receptor-mediated endocytosis of pneumococci into epithelial and endothelial cells.

192 locyte recruitment with an earlier spread of pneumococci into the bloodstream, compared with wild-typ

193 al colonization or that acquired immunity to pneumococci is an accumulation of individually weak resp

194 y intranasal vaccination of mice with killed pneumococci is mediated by T(H)17 cells and correlates w

195 opulation composed of primarily opaque-phase pneumococci is released only by homogenization of the na

196 A paradigm for pneumococci is their interaction with the adhesive glyco

197 s ability to modulate the immune response to pneumococci is unknown.

198 protein A (PspA), a major surface protein of pneumococci, is a promising vaccine target.

199 vasive disease, defined as disease caused by pneumococci isolated from a normally sterile site, were

200 ntegrated within the bacterial genome) among pneumococci isolated over the past 90 years.

201 After microbiological identification as pneumococci, isolates (n = 1,135) were serotyped using l

202 ytometry to measure antibody binding to live pneumococci, it was observed that the mice that survived

203 vaccine-type (VT) and non-vaccine-type (NVT) pneumococci; it decreased with age (P < .001 for VT and

204 e I IFN receptor, or in mice challenged with pneumococci lacking pneumolysin.

205 Pneumococci lacking RafK showed a 50- to 80-fold reducti

206 not as attenuated as DLDH-negative bacteria, pneumococci lacking RafK were significantly outcompeted

207 istorically associated with vaccine-serotype pneumococci may impact the susceptibility of children to

208 tes in the normal human airway suggests that pneumococci must utilize complex glycan structures for g

209 hich we used 150 mug of CRP and 10(7) CFU of pneumococci, mutant CRP was as protective as wild-type C

210 h we used 25 mug of CRP and 5 x 10(7) CFU of pneumococci, mutant CRP was not protective while wild-ty

211 When immunized with live attenuated pneumococci, mutant mice mounted robust antibody respons

212 In general, new acquisition of pneumococci nonsusceptible to penicillin, erythromycin,

213 ality draft genomes from 265 isolates of NVT pneumococci not susceptible to penicillin (PNSP) in 2009

214 assay, we examined 495 clinical isolates of pneumococci obtained in Brazil, Denmark, and Mexico.

215 mplies that intraspecies competition between pneumococci occurs during nasopharyngeal colonization, a

216 ymphocyte-dependent accelerated clearance of pneumococci of various serotypes from the nasopharynx me

217 ividuals differ in their natural exposure to pneumococci or have altered mucosal immune responses aft

218 lial cell monolayers in vitro in response to pneumococci or hepoxilin-A3, an eicosanoid required for

219 ophages when rBPI21 was combined with killed pneumococci or supernatant from overnight growth of pneu

220 , or rayon-tipped swabs were inoculated with pneumococci or were immersed in nasal wash specimens fro

221 ut were more likely to be colonized with NVT pneumococci (OR, 1.67 [95% CI, 1.02-2.78]).

222 s, differing proportions of pneumonia due to pneumococci, or data limitations.

223 It has been postulated that pneumococci persist in vivo in biofilm communities.

224 We also show that pneumococci primarily localize to the olfactory bulb, le

225 rum, complement component C3 is deposited on pneumococci primarily via the classical pathway.

226 -) mice that were infected intranasally with pneumococci rapidly succumbed, with 80% mortality after

227 In summary, pneumococci recognition induces a negative feedback loop

228 nfection, from 24 hours onward the number of pneumococci recovered from lungs and distant body sites

229 that sialic acid can increase the number of pneumococci recovered from the olfactory bulbs and brain

230 elial cells and is the main pathway by which pneumococci reduce surface bound capsule during early ac

231 ignificantly reduced in vitro AMo killing of pneumococci, relative to other conditions, in part by de

232 If the opaque-phase pneumococci released from the nasal tissue were from wit

233 ptococcus pneumoniae is limited, even though pneumococci rely on efficient acquisition and metabolism

234 Incubation of apolactoferrin with growing pneumococci resulted in a 12-kDa reduction in its molecu

235 primary blood-derived human macrophages with pneumococci resulted in transcriptional changes in sever

236 Mild respiratory infection with serotype 19F pneumococci selectively induced systemic anti-dsDNA IgA

237 ession of raf operon genes, as DLDH-negative pneumococci showed a significantly decreased expression

238 eq) analyses of planktonic and biofilm-grown pneumococci showed that metabolic pathways involving the

239 hus, exposure of neonatal mice to PC-bearing pneumococci significantly reduced the development of HDM

240 ion), they are cleared faster than opsonized pneumococci similarly injected with wild-type mouse eryt

241 Taken together, pneumococci specifically interact with human C4BP via en

242 both HAMLET- and starvation-induced death of pneumococci specifically required a sodium-dependent cal

243 e obtained from three gram-positive species (pneumococci, staphylococci, and group B streptococci) du

244 Morphine treatment reduced MIP-2 release in pneumococci stimulated alveolar macrophages.

245 10 bound to wild type but not psrP deficient pneumococci; suggesting that unlike other serine-rich re

246 on with antimicrobial peptides, encapsulated pneumococci survive by removing capsule from the cell su

247 In a mouse pneumonia model, more susceptible pneumococci survive Cm treatment when coinfected with a

248 th PiuA and PiaA were present in all typical pneumococci tested, (covering 20 and 27 serotypes, respe

249 produces LTA that is more representative of pneumococci than that previously characterized from the

250 e reversed by activation of macrophages with pneumococci that are high NF-kappaB activators.

251 We sought to assess whether pneumococci that are nontypeable (NT) by the Quellung re

252 Our data suggest that disease is caused by pneumococci that are primed to move to tissue sites with

253 cs are well defined, it is not clear whether pneumococci that cause meningitis are genetically distin

254 ere chains of variable lengths; however, the pneumococci that entered the brain were division-compete

255 ci, there are several reports of nontypeable pneumococci that give inconsistent results with one or m

256 We conclude that pneumococci that have invaded the myocardium are an impo

257 e does not explain the virulence behavior of pneumococci that reach the meninges.

258 Pneumococci that try to invade the lower airways are rec

259 eptors involved in direct binding of RSV and pneumococci, the effects of which were studied in both i

260 tandards for identifying and differentiating pneumococci, there are several reports of nontypeable pn

261 selves from "extracellular" bacteria such as pneumococci, there is little direct evidence.

262 By improving the adherence of pneumococci, this prophage may contribute to their fitne

263 ntibody may also facilitate the clearance of pneumococci through immune adherence.

264 The capacity of pneumococci to adhere to and infect lower airway cells i

265 that sialic acid can enhance the ability of pneumococci to disseminate into the CNS and provide deta

266 We identify the ability of pneumococci to drive TGF-beta1 production from nasophary

267 PspK increased binding of pneumococci to epithelial cells and enhanced pneumococca

268 n enhances the immune adherence of opsonized pneumococci to erythrocytes in vitro, and the pneumococc

269 SP-1 to the bacterial surface and binding of pneumococci to host cell-bound hTSP-1 during adhesion.

270 f PspC with FH may also mediate adherence of pneumococci to human cells.

271 The ability of pneumococci to make PcpA negatively modulated both the i

272 istological changes show that the ability of pneumococci to make PcpA was associated with unresolved

273 arance function of these molecules, allowing pneumococci to persist in the airway.

274 utilization locus and imparts the ability of pneumococci to utilize inulin.

275 ontribute to the adherence of unencapsulated pneumococci, to human epithelial cells.

276 hway that was previously shown to bind ST11A pneumococci, to recognize and mediate complement-depende

277 sm of pneumococcal-host interaction, whereby pneumococci use a host complement protein C1q, primarily

278 Pneumococci utilize at least 32 carbohydrates in vitro.

279 es, we hypothesized that during colonization pneumococci utilize the released carbohydrates for growt

280 olar macrophages stimulated with heat-killed pneumococci was enhanced by IFN-gamma, and TNF-alpha in

281 of pediatric pneumonia caused by serotype 5 pneumococci was identified in a northeast London suburb.

282 and subsequently decreased C3b deposition on pneumococci was observed.

283 Pneumococci were collected after 2 hours exposure and ch

284 Swabs and medium inoculated with pneumococci were cultured.

285 Cocolonizing pneumococci were less bactericidal and cocolonizing stap

286 Pneumococci were present within surface-attached biofilm

287 Pneumococci were serotyped and tested for antibiotic sus

288 Pneumococci were serotyped by the Neufeld test in their

289 Pneumococci were serotyped by the Quellung reaction.

290 Pneumococci were the leading pathogen identified in 76 o

291 subset important in protecting mice against pneumococci, were also depleted following immunization w

292 Such immune pressure may select for pneumococci, which avoid or subvert macrophage NF-kappaB

293 ed macrophages generated mROS in response to pneumococci, which colocalized with bacteria and phagoly

294 ) mice were immunized with heat-inactivated pneumococci, which were shown to induce the production o

295 This finding strongly suggests that the pneumococci with high transformation capability are "add

296 may create a selective environment favoring pneumococci with immune-evasive phenotypes.

297 rBPI21 also enhanced the association of pneumococci with murine macrophages.

298 surface-exposed proteins, as pretreatment of pneumococci with pronase E but not sodium periodate sign

299 e sequence was similar in structure to other pneumococci, with the exception of a 100 kb inversion.

300 BrdU confirmed intracellular replication of pneumococci within HL-1 cells.