ライフサイエンスコーパス: pneumococci

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

2 ntibodies mediate the killing of serotype 6E pneumococci.

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

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

5 in vitro mediator production to heat-killed pneumococci.

6 for both meningitis- and bacteremia-causing pneumococci.

7 toms of diseases potentially attributable to pneumococci.

8 he activation of purified human platelets by pneumococci.

9 nasopharyngeal carriage of vaccine-serotype pneumococci.

10 that have not been described in encapsulated pneumococci.

11 umbers, is crucial for prolonged carriage of pneumococci.

12 actor predicting antimicrobial resistance in pneumococci.

13 fection favors nasopharyngeal acquisition of pneumococci.

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

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

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

17 purified C1q to various clinical isolates of pneumococci.

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

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

20 high rates of nasopharyngeal acquisition of pneumococci.

21 nventional de novo biosynthesis of serine by pneumococci.

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

23 (95% CI 26.7-46.1) for vaccine serotype (VT) pneumococci.

24 ecting for the outgrowth of CRISPR-defective pneumococci.

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

26 2 isolates previously labeled as nontypeable pneumococci.

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

28 splay higher antibody concentrations against pneumococci.

29 expression induced by lipoteichoic acid and pneumococci.

30 over, and 4 weeks later challenged mice with pneumococci.

31 d not the intact apolactoferrin, which kills pneumococci.

32 tself rapidly clear small initial numbers of pneumococci.

33 dynamics and improved interventions against pneumococci.

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

35 mulating the killing of complement-opsonized pneumococci.

36 the upper airway lumen, where they engulfed pneumococci.

37 6A, 6B, 6C, and 19A but did not opsonize 19F pneumococci.

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

39 atory circuits for lung-specific invasion by pneumococci.

40 first line of defense against invading lung pneumococci.

41 n against CAAP attributable to PCV7-serotype pneumococci.

42 icillin-resistant and erythromycin-resistant pneumococci.

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

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

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

46 secondary bacterial infections, primarily by pneumococci.

47 toms of diseases potentially attributable to pneumococci.

48 n rapid immune exclusion of pilus-expressing pneumococci.

49 c infection and transform into more virulent pneumococci.

50 analysis was conducted for the non-typeable pneumococci.

51 essential for the transformation process in pneumococci.

52 unknown - role in protein phosphorylation in pneumococci.

53 the efficacy of opsonophagocytic killing of pneumococci.

54 nate asymptomatic carriage with vaccine-type pneumococci.

55 ining samples seemed to contain non-typeable pneumococci (0.8%), and non-pneumococci positive for lyt

56 A collection of 150 pneumococci, 433 non-pneumococci and 240 polymicrobial s

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

58 compared to those infected by non-pbp1b641C pneumococci, after controlling for pneumococcal serotype

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

60 Dispersed pneumococci also upregulated genes associated with produ

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

62 A collection of 150 pneumococci, 433 non-pneumococci and 240 polymicrobial samples (obtained from

63 confidence interval [CI] 10.6-21.8) for all pneumococci and 39.2% (95% CI 26.7-46.1) for vaccine ser

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

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

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

67 herence required interaction of agglutinated pneumococci and entrapment in mucus particles.

68 analysis revealed that TF is conserved among pneumococci and has no human homologue.

69 Pneumococci and nontypeable Haemophilus influenzae (NTHi

70 plications for future vaccine design against pneumococci and other pathogens.

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

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

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

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

75 against CAAP attributable to PCV13-serotype pneumococci, and 92.3% (-0.9-100.0%) protection against

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

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

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

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

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

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

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

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

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

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

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

87 Pneumococci are potent inducers of neutrophil degranulat

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

89 Pneumococci are transported from the nasopharynx to the

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

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

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

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

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

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

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

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

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

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

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

101 300) homes were screened for the presence of pneumococci by qPCR targeting lytA and piaB.

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

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

104 Pneumococci can switch capsules, evading vaccine pressur

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

106 y detecting additional vaccine serotype (VT) pneumococci carried at low relative abundances (median,

107 Pneumococci cause meningitis by invading the blood and p

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

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

110 Serotype 11A pneumococci characteristically express capsule beta-gala

111 Analyzing pneumococci collected from children in Massachusetts, we

112 In mice, PLY-expressing pneumococci colocalize with MRC-1 in alveolar macrophage

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

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

115 It is challenging to study how pneumococci control virulence factor expression, because

116 Pneumococci could evade pneumococcal conjugate vaccines

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

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

119 tal number of isolates and vaccine-type (VT) pneumococci decreased from PreVac to PostVac-II (n = 314

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

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

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

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

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

125 As pneumococci do not produce catalase or an inducible regu

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

127 Pneumococci engage vitronectin, the human adhesive glyco

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

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

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

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

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

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

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

135 Thus, pneumococci express a versatile repertoire of surface pr

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

137 ng to increasing disease incidence caused by pneumococci expressing non-vaccine serotypes.

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

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

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

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

142 as sent to the National Reference Center for Pneumococci for serotyping.

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

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

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

146 The genomes represented pneumococci from before and after pneumococcal conjugate

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

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

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

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

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

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

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

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

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

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

157 Pneumococci harboring these genes show increased growth

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

159 Pneumococci have evolved several strategies to circumven

160 Pneumococci have evolved several strategies to evade the

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

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

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

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

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

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

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

168 hin-host microevolution of naturally carried pneumococci in ninety-eight infants intensively sampled

169 Use of qPCR improved detection of pneumococci in oropharyngeal samples compared to CCBM: f

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

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

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

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

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

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

176 neumococcal strains; piaB was absent in some pneumococci including a serotype 6B strain.

177 ], respectively), but non-vaccine-type (NVT) pneumococci increased among adults 18 to 64 years old (n

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

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

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

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

182 46a as one putatively important regulator of pneumococci-induced host cell activation.

183 The pneumococci-induced oxidative stress was independent of

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

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

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

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

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

189 Why some pneumococci invade the bloodstream or CSF (so-called inv

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

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

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

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

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

195 Pneumococci isolated between 2009 and 2017 at the Landsp

196 enetic lineages, and antimicrobial-resistant pneumococci isolated from the lower respiratory tract (L

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

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

199 al (adults only) swabs underwent culture for pneumococci; isolates were serotyped.

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

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

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

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

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

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

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

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

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

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

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

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

212 CV) has brought about a dramatic decrease in pneumococci of vaccine serotypes (VTs) but nonvaccine se

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

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

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

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

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

218 rom 2009 and 2013; penicillin nonsusceptible pneumococci (PNSP) was defined as penicillin-intermediat

219 ain non-typeable pneumococci (0.8%), and non-pneumococci positive for lytA (1.7%) or SP2020 (8.7%).

220 burdens in murine tissues when infected with pneumococci pre-incubated with influenza virus versus co

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

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

223 Moreover, serotype 7F pneumococci produced much less CPS than strains of other

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

225 In summary, pneumococci recognition induces a negative feedback loop

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

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

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

229 ppreciably between colonizing and AC-causing pneumococci, regardless of NTHi co-occurrence.

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

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

232 c pneumonia attributable to vaccine-serotype pneumococci remains unknown.

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

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

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

236 nicillin-susceptible or penicillin-resistant pneumococci (serotypes 3 and 14, respectively).

237 Patients infected by the pbp1b641C genotype pneumococci show 2.8-fold odds (95% CI 1.7 to 4.8) of me

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

257 Pneumococci that try to invade the lower airways are rec

258 elial cells are among the first to encounter pneumococci, the cellular processes and contribution of

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

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

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

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

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

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

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

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

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

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

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

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

274 In conclusion, we show that pneumococci use PLY-MRC-1 interactions to downregulate i

275 Pneumococci utilize at least 32 carbohydrates in vitro.

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

277 gainst CAAP attributable to vaccine-serotype pneumococci via the joint reduction in risks of carriage

278 tection against carriage of vaccine-serotype pneumococci via the relative risk of detecting these ser

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

280 and subsequently decreased C3b deposition on pneumococci was observed.

281 Pneumococci were collected after 2 hours exposure and ch

282 Swabs and medium inoculated with pneumococci were cultured.

283 Pneumococci were detected by means of broth-enrichment c

284 Nasopharyngeal pneumococci were molecular-serotyped by microarray.

285 st the effect of these interactions in vivo, pneumococci were preincubated with human sIgA before int

286 Pneumococci were present within surface-attached biofilm

287 Pneumococci were serotyped and tested for antibiotic sus

288 Pneumococci were serotyped by the Quellung reaction.

289 Pneumococci were the leading pathogen identified in 76 o

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

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

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

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

294 Treatment of pneumococci with HAMLET immediately inhibited their ATP

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

298 Five lung aspirates cultured pneumococci, with a matching strain identified in the na

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.