ライフサイエンスコーパス: S. pneumoniae

1 S. pneumoniae colonization was not significantly associa

2 S. pneumoniae D39 derivatives with defined deletion or p

3 S. pneumoniae density was substantially higher in vaccin

4 S. pneumoniae established effective commensal colonizati

5 S. pneumoniae infection augments atherosclerosis and exa

6 S. pneumoniae infection triggered atherogenesis, led to

7 S. pneumoniae invades the myocardium and induces cardiac

8 S. pneumoniae isolates were serotyped and tested for ant

9 S. pneumoniae that colonized the respiratory epithelium

10 S. pneumoniae was detected in the myocardium of all NHPs

11 S. pneumoniae was identified using microbiological cultu

12 S. pneumoniae was the most common pathogen detected (n =

13 S. pneumoniae, Entrobacter species, K. pnemoniae and H.

14 S. pneumoniae-mediated PAF deprivation impaired viabilit

15 ia coli isolates by MIC and 30 S. aureus, 15 S. pneumoniae, and 15 S. pyogenes isolates by disk diffu

16 uency and other associated phenotypes of 208 S. pneumoniae clinical isolates representing at least 30

17 ity to respiratory infection with serotype 3 S. pneumoniae relative to younger adult mice, regardless

18 value identification identified correctly 46 S. pneumoniae and 4 S. pseudopneumoniae but misidentifie

19 istant sequence type 156 (ST156) serotype 9V S. pneumoniae in 3 respiratory patients that resulted in

20 A S. pneumoniae thioesterase (TesS, SP1408) hydrolyzed acy

21 and acute kidney injury in a patient with a S. pneumoniae infection.

22 hibited their antibacterial activity against S. pneumoniae but did not affect their ability to activa

23 all displayed bactericidal activity against S. pneumoniae, but only CCL26 and CCL28 retained high an

24 termine the role of human antibodies against S. pneumoniae protein vaccine candidates PhtD, PcpA, and

25 L1 and CXCL5, improves host defenses against S. pneumoniae.

26 uding Streptococcus pyogenes, S. agalactiae, S. pneumoniae, and S. equi.

27 spectra evaluation correctly identified all S. pneumoniae and S. pseudopneumoniae strains but miside

28 ults provide a correct identification of all S. pneumoniae and S. pseudopneumoniae isolates.

29 red by PAF and the bacterial cell wall allow S. pneumoniae to leverage a ChoP-remodeling enzyme (Pce)

30 These residues are highly conserved among S. pneumoniae Cps2E homologues, and mutations therein se

31 studied histidine triad protein D (PhtD), an S. pneumoniae adhesin vaccine candidate, for its ability

32 mice from septicemia caused by S. aureus and S. pneumoniae, whereas untreated mice die within 24-33 h

33 nt of the DeltaplsX strains of S. aureus and S. pneumoniae.

34 V is altered in mice coinfected with IAV and S. pneumoniae and that this response differs, depending

35 reaction assays quantified H. influenzae and S. pneumoniae and confirmed H. influenzae as nontypeable

36 m and pH 5.5 (no growth of H. influenzae and S. pneumoniae by BMD).

37 ording protection against N. menigitidis and S. pneumoniae.

38 % CI = 1.29-4.88; n = 921 participants), and S. pneumoniae community-acquired pneumonia (OR = 2.15; 9

39 l and laboratory isolates of S. pyogenes and S. pneumoniae as both organisms are thought to colonize

40 Coinfection with RSV and S. pneumoniae is associated with severe and often fatal

41 neuraminidase-expressing influenza virus and S. pneumoniae potentiates both colonization and infectio

42 interaction between respiratory viruses and S. pneumoniae in CAAP pathogenesis.

43 tic fluoroquinolone-resistant MRSA, VRE, and S. pneumoniae, and the possibility to offer patients an

44 hus, MARCO is an important component of anti-S. pneumoniae responses in the murine nasopharynx during

45 mococcal isolates (<1%) was misidentified as S. pneumoniae.

46 ocus of public health strategies directed at S. pneumoniae.

47 iations in sensitivity to complement between S. pneumoniae capsular serotypes could affect invasivene

48 el, in which significant differences between S. pneumoniae TIGR4 and the capsule-switching mutant wer

49 or the immunochromatographic (ICT) BinaxNow S. pneumoniae test (composite diagnostic) was positive.

50 acological inhibition of this enzyme blocked S. pneumoniae-induced PMN transepithelial migration in v

51 ly provides protective immunity against both S. pneumoniae and influenza virus.

52 sly confers protective immunity against both S. pneumoniae and influenza virus.

53 d functional changes in the biofilms of both S. pneumoniae and S. aureus.

54 ve transforming growth factor (TGF)-beta1 by S. pneumoniae in human host cells and highlight the key

55 y the role of MCs during pneumonia caused by S. pneumoniae.

56 xacerbates nasal colonization and disease by S. pneumoniae, in part via the synergistic contributions

57 and the most prevalent sugar encountered by S. pneumoniae during invasive disease.

58 ssion and middle ear inflammation induced by S. pneumoniae and reduced hearing loss and pneumococcal

59 thophysiology of oxidative stress induced by S. pneumoniae and the role of nuclear factor erythroid 2

60 ant induction of oxidative stress induced by S. pneumoniae in vivo, ex vivo, and in vitro.

61 Colonization of the nasopharynx by S. pneumoniae precedes pulmonary and other invasive dise

62 with acute pneumonia, and H2O2 production by S. pneumoniae in vivo contributes to its genotoxicity an

63 tibodies against host proteins recognized by S. pneumoniae adhesins, we showed that S. pneumoniae upt

64 geal colonisation model, black carbon caused S. pneumoniae to spread from the nasopharynx to the lung

65 tion, and influenza virus coinfection caused S. pneumoniae NP density to increase, resulting in bacte

66 sis of 271 strains of conjunctivitis-causing S. pneumoniae from 72 postal codes in the United States.

67 All blood samples with >/= 10(3)CFU S. pneumoniae per ml of human blood were successfully de

68 absence of Pce, neutrophils rapidly cleared S. pneumoniae from the airway and impeded invasive disea

69 The TAC method was evaluated on 146 clinical S. pneumoniae isolates and 13 nonpneumococcal species th

70 such as influenza A virus, induces commensal S. pneumoniae to disseminate beyond the nasopharynx and

71 Consistently, S. pneumoniae D39 caused higher cytotoxicity to RAW 264.

72 utrophils were indispensable for controlling S. pneumoniae outgrowth but contributed to alveolar barr

73 The DeltaplsX S. pneumoniae strain was refractory to myristic acid-dep

74 Different S. pneumoniae strains caused distinct cardiac pathologie

75 and mouse lungs were infected with different S. pneumoniae strains (D39, A66, R6x, H2O2/pneumolysin/L

76 ng described in this study can differentiate S. pneumoniae from other Streptococcus species.

77 -off absorbance-value of 2.1, differentiated S. pneumoniae from all but one other mitis group strepto

78 uring both colonization and invasive disease S. pneumoniae ferments host-derived carbohydrates as its

79 During invasive pneumococcal disease, S. pneumoniae can gain access to the myocardium, kill ca

80 ed with biofilm bacteria, actively dispersed S. pneumoniae, which were more virulent in invasive dise

81 data demonstrate a key role for PAR-1 during S. pneumoniae lung infection that is mediated, at least

82 genes-mediated production of IFN-beta during S. pneumoniae infection is decreased in aged hosts.

83 of PLA2 in local and systemic disease during S. pneumoniae infection.

84 oll-like receptor 5 agonist flagellin during S. pneumoniae challenge exacerbated IL-22 production by

85 As (miRs) in lung neutrophils in mice during S. pneumoniae pneumonia and performed in depth in silico

86 protected from lethal challenge with either S. pneumoniae or influenza virus.

87 on with a high-dose inoculum of encapsulated S. pneumoniae, alveolar macrophage-independent clearance

88 pid bacterial replication, with an estimated S. pneumoniae doubling time of 16 min.

89 Moreover, in the presence of ethanol, S. pneumoniae AdhE produced acetaldehyde and NADH, which

90 ired for lethal systemic infection following S. pneumoniae lung challenge.

91 with pneumonia who had positive cultures for S. pneumoniae from January 1, 2000 to December 31, 2013.

92 stantially different from that described for S. pneumoniae at other infection sites.

93 f PAF signaling rendered Pce dispensable for S. pneumoniae persistence, reinforcing that this enzyme

94 nal differences are apparent, especially for S. pneumoniae.

95 Of 643 patients hospitalized for S. pneumoniae pneumonia, 139 (22%) were macrolide resist

96 d here confirm the importance of pilus I for S. pneumoniae pathogenesis and the potential use of anti

97 Hence, LTA is important for S. pneumoniae to establish systemic infections, and TacL

98 aecalis ATCC 29212, 0.008 to 0.03 mug/ml for S. pneumoniae ATCC 49619, and 2 to 8 mug/ml for H. influ

99 mm for S. aureus ATCC 25923, 25 to 31 mm for S. pneumoniae ATCC 49619, and 16 to 20 mm for H. influen

100 ): of 35 samples that were qPCR positive for S. pneumoniae, N. meningitidis, and H. influenzae, only

101 A model is proposed for S. pneumoniae SczA function in which both A- and B-sites

102 been identified as nonopsonic receptors for S. pneumoniae in the lung, we used scavenger receptor kn

103 Of these, 749 (77%) had blood tested for S. pneumoniae.

104 es and also with potassium and thymidine for S. pneumoniae For all other variations, gepotidacin MIC

105 s proteins, which are themselves absent from S. pneumoniae.

106 and coculture of these respective APCs from S. pneumoniae- or OVA-immunized mice with OVA-specific T

107 w family 20 glycoside hydrolase, GH20C, from S. pneumoniae.

108 creased more than 2-fold in neutrophils from S. pneumoniae pneumonia.

109 drate-binding module (CBM), originating from S. pneumoniae, with a synthetic B type 2 neoglycolipid,

110 comprehensive model of the type 1 pilus from S. pneumoniae is also presented.

111 vide immediate and essential protection from S. pneumoniae through production of natural Ig, which ha

112 age of the glycosidic bonds in host glycans, S. pneumoniae deploys a wide array of glycoside hydrolas

113 ern because - in contrast to HRSV and HMPV - S. pneumoniae can become part of the nasopharyngeal flor

114 We sought to determine how S. pneumoniae coinfection modulates the B cell immune re

115 ced sustained pulmonary infection by a human S. pneumoniae isolate in naive and comorbid rodents to i

116 enotypic TaqMan array card (TAC) to identify S. pneumoniae strains, including lytA-based sequences, a

117 he A- and B-site SczA mutant variants impact S. pneumoniae resistance to zinc toxicity and survival i

118 Importantly, S. pneumoniae induces DSBs in the lungs of animals with

119 In S. pneumoniae, nearly 100% of cells that were recovered

120 tial role for neutrophil-derived IL-1beta in S. pneumoniae infection, and they elucidate the role of

121 , while such patterns were largely absent in S. pneumoniae.

122 ntified a c-di-AMP binding protein (CabP) in S. pneumoniae using c-di-AMP affinity chromatography.

123 atile surveyor of available carbohydrates in S. pneumoniae.

124 upport for the hypothesis that competence in S. pneumoniae is regulated in response to the accumulate

125 highly regulated step of gene expression in S. pneumoniae.

126 nly a partial rethink of septum formation in S. pneumoniae, but consideration of the modes of PBP loc

127 egrated into the CCR regulatory framework in S. pneumoniae.

128 major and possibly sole function of GreA in S. pneumoniae is to prevent formation of backtracked elo

129 iptional characteristics of the cps locus in S. pneumoniae.

130 ow that generation of a mutator phenotype in S. pneumoniae through deletions of mutX, hexA or hexB en

131 We test these predictions in S. pneumoniae and find that the duration of carriage of

132 Zinc intoxication is prevented in S. pneumoniae by expression of the zinc exporter CzcD, w

133 caused a significant (P < 0.05) reduction in S. pneumoniae colonization.

134 ism of failure of Th17 immunity resulting in S. pneumoniae infections in children <2 years old.

135 The expression of SPD_0247 in S. pneumoniae harvested from infected tissues was signif

136 is shown here through functional studies in S. pneumoniae that an unannotated homodimeric TetR from

137 hanism for a Phr-peptide signaling system in S. pneumoniae and found that it induces the expression o

138 e against extracellular pathogens, including S. pneumoniae, we hypothesized that ethanol impairs muco

139 Indeed, S. pneumoniae invasion of HL-1 cells occurred through cl

140 ivative of the alkaloid vincamine, inhibited S. pneumoniae-induced mucin MUC5AC upregulation in cultu

141 derived cells, depleted by CLs, internalized S. pneumoniae in vivo, whereas CD11c(low) dendritic cell

142 d, the initial interactions of heart-invaded S. pneumoniae with cardiomyocytes remain unclear.

143 utcome with regard to prevention of invasive S. pneumoniae pathogenesis with a protein vaccine simila

144 ndidate, for its ability to prevent invasive S. pneumoniae disease in adult and infant mice.

145 rrow neutrophils stimulated with heat-killed S. pneumoniae (signal 1) and pneumolysin (signal 2) exhi

146 s of IP children stimulated with heat-killed S. pneumoniae had significantly reduced percentages of C

147 attenuated TLR2-associated responses to lgt S. pneumoniae, comprising many NF-kappaB-regulated proin

148 ters when immunized and challenged with live S. pneumoniae infection.

149 NA copies per LAMP zone for N. meningitidis, S. pneumoniae and Hib were achieved within 1h.

150 e presence of interesting antibacterial [MIC(S. pneumoniae) approximately 1.2 muM] and anticancer [IC

151 In all models, S. pneumoniae TIGR4 showed higher rates of survival than

152 actiae, S. dysgalactiae, S. equi, S. mutans, S. pneumoniae, S. suis and S. uberis, as well as represe

153 red with other unencapsulated nasopharyngeal S. pneumoniae.

154 To mimic natural S. pneumoniae pathogenesis, we commensally colonized the

155 IRRs for single NTHi, mixed NTHi + S. pneumoniae, and all-NTHi OM were 0.30 (0.25-0.35), 0.

156 ly correlated with the relative abundance of S. pneumoniae.

157 nother tool that is unique in the arsenal of S. pneumoniae and that it may implement the effort of th

158 cifically affecting the adhesive capacity of S. pneumoniae led to the identification of the monoclona

159 ment but did not influence total carriage of S. pneumoniae, H. influenzae, or S. aureus.

160 ntially contributed to the observed cases of S. pneumoniae-positive CAP or HCAP.

161 Clearance of S. pneumoniae from lungs of HbSS mice or C57BL/6 mice wa

162 roles of these receptors in the clearance of S. pneumoniae from the nasopharynx.

163 mice had significantly impaired clearance of S. pneumoniae from the nasopharynx.

164 hat CozE is a member of the MreCD complex of S. pneumoniae that directs the activity of PBP1a to the

165 at qPCR significantly increases detection of S. pneumoniae, N. meningitidis, and H. influenzae in CSF

166 p streptococci, including differentiation of S. pneumoniae from Streptococcus pseudopneumoniae.

167 hallenged intranasally with a lethal dose of S. pneumoniae D39.

168 roteins are involved in the encapsulation of S. pneumoniae in a posttranscriptional manner.

169 th cases and controls, with the exception of S. pneumoniae in exposed controls, which was detected 25

170 molysin (PLY) is a major virulence factor of S. pneumoniae and a target for both small molecule drug

171 ells via the release of bacterial factors of S. pneumoniae.

172 aracterized the c-di-AMP-associated genes of S. pneumoniae.

173 The impact of S. pneumoniae on host molecular processes that lead to d

174 -induced oxidative stress was independent of S. pneumoniae-derived H2O2 and pneumolysin but depended

175 The intracerebral injection of S. pneumoniae D39 induced the recruitment of B and T cel

176 nia was induced by intranasal inoculation of S. pneumoniae.

177 on of pneumonia by intranasal inoculation of S. pneumoniae.

178 studied at 6 and 24 h after instillation of S. pneumoniae or PBS.

179 d whole-genome sequencing of 140 isolates of S. pneumoniae recovered from bloodstream infection (n =

180 Although the peptidoglycan layer of S. pneumoniae tolerates a combination of both branched a

181 quisition of the serotype 4 capsule locus of S. pneumoniae TIGR4, following induction of competence f

182 le cocci, suggesting that only a minority of S. pneumoniae are poised to cross the BBB.

183 Using a murine model of S. pneumoniae corneal infection, we demonstrated a requi

184 We have used a murine model of S. pneumoniae early lung infection with wild-type, unenc

185 ral role in cytokinesis and morphogenesis of S. pneumoniae.

186 tudy, we used a model of low multiplicity of S. pneumoniae infection with HL-1 mouse cardiomyocytes t

187 with implications in the pathophysiology of S. pneumoniae infection.

188 During the acute phases of S. pneumoniae infection, these populations of splenic ne

189 as observed with regard to the prevention of S. pneumoniae bacteremia, and there was no difference in

190 mediating the immunosuppressive property of S. pneumoniae.

191 n patients with pneumonia, the proportion of S. pneumoniae-specific plasmablasts expressing L-selecti

192 ion with PCV13 led to a greater reduction of S. pneumoniae NP density (>2.5 log units) than PhtD vacc

193 s, a human commensal and a close relative of S. pneumoniae, was also shown to have a capsule.

194 s, attesting to intracellular replication of S. pneumoniae as a key first step in pneumococcal pathog

195 ressure by human CMV and the 23F serotype of S. pneumoniae acted on the IGVK3-11 and IGVH3-30 genes a

196 o both an invasive and noninvasive strain of S. pneumoniae (D39 and EF3030) but that PAR-1 antagonism

197 , we compared an isogenic deletion strain of S. pneumoniae TIGR4 in polyamine transport operon (Delta

198 We sequenced and serotyped 349 strains of S. pneumoniae isolated from IPD patients in Nijmegen bet

199 ent study, comparative structural studies of S. pneumoniae CPS serogroup 10 (CPS10) were extended to

200 d have important implications for studies of S. pneumoniae pathogenesis.

201 nate lyase (Hyl) presented on the surface of S. pneumoniae performs this role.

202 wofold higher expression compared to that of S. pneumoniae R6, could also confer increased resistance

203 tic activity, colonization, and virulence of S. pneumoniae, as well as host cell myeloperoxidase acti

204 opsonic capacity by increasing C3 binding on S. pneumoniae Taken together, endogenous IL-22 and hepat

205 n, and cutaneous lymphocyte antigen (CLA) on S. pneumoniae-specific plasmablasts was examined in pati

206 lide use and PCV7 and PCV13 introductions on S. pneumoniae were associated with changes in macrolide

207 t in one of the CBPs, demonstrated that only S. pneumoniae lacking the CBP pneumococcal surface prote

208 s after intratracheal instillation of PBS or S. pneumoniae, and differentially expressed (DE) mRNAs a

209 (N. meningitidis), Streptococcus pneumoniae (S. pneumoniae), and Haemophilus influenzae type b (Hib)

210 False-positive S. pneumoniae results may warrant reporting of only "Str

211 g the importance of DNA repair in preventing S. pneumoniae-induced genotoxicity.

212 ultiple independent transformations produced S. pneumoniae R6 derivatives containing murEUo5 , pbp2xU

213 using microbiological cultures, BinaxNOW(R) S. pneumoniae assay, or urine antigen detection (UAD) as

214 were extended to include genetically related S. pneumoniae CPS34, CPS39, and CPS47F.

215 increased circulation of macrolide-resistant S. pneumoniae carriage among young children in the 6 mon

216 atients hospitalized for macrolide-resistant S. pneumoniae pneumonia were more severely ill on presen

217 invasive or noninvasive) macrolide-resistant S. pneumoniae pneumonia, and no effect on outcomes as a

218 In contrast, secondary S. pneumoniae infection exaggerates early antiviral anti

219 of a MassTag PCR assay designed to serotype S. pneumoniae and demonstrate its utility in tests using

220 ions (M-OM) and those with OM due to single, S. pneumoniae-only infections (S-OM) and to examine whet

221 te vaccines to prevent non-serotype-specific S. pneumoniae colonization and invasive infection.

222 riments with the sensitive laboratory strain S. pneumoniae R6 as recipient.

223 els lower than those for the virulent strain S. pneumoniae TIGR4.

224 , which neutralizes H2O2, greatly suppresses S. pneumoniae-induced DNA damage and apoptosis.

225 populations and MZ B cells regulate systemic S. pneumoniae clearance through complementary mechanisms

226 and its lipoteichoic acid, demonstrate that S. pneumoniae binds to cells via its phosphocholine resi

227 The fact that S. pneumoniae, H. influenzae, and S. aureus polymicrobia

228 contractility; (2) the new observation that S. pneumoniae is capable of translocation into the myoca

229 We observed that S. pneumoniae mutants deficient in NanA and beta-galacto

230 orescence microscopy (IFM), we observed that S. pneumoniae replication within the heart preceded visu

231 Here, we show that S. pneumoniae induces toxic DNA double-strand breaks (DS

232 smission electron microscopy, we showed that S. pneumoniae rapidly adhered to and invaded cardiomyocy

233 ed by S. pneumoniae adhesins, we showed that S. pneumoniae uptake by cardiomyocytes is not through th

234 Taken together, this study shows that S. pneumoniae-induced damage to the host cell genome exa

235 al doubling time increased to 56 min and the S. pneumoniae alveolar macrophage-dependent clearance ha

236 shotgun sequencing (RNA-seq) to compare the S. pneumoniae transcriptome in biofilms, bacteria disper

237 hanced in the S. mitis strain expressing the S. pneumoniae capsule, which showed, in addition, increa

238 r haptenic component of teichoic acid in the S. pneumoniae cell wall, and lipoteichoic acid in the S.

239 niae cell wall, and lipoteichoic acid in the S. pneumoniae membrane were previously reported to be im

240 eptococcus pneumoniae Some components of the S. pneumoniae glycoconjugate vaccine Prevnar13 that cont

241 Here, we showed that the S. pneumoniae type 2 D39 strain is ethanol tolerant and

242 Thus, S. pneumoniae arginine synthesis genes promote growth an

243 Thus, S. pneumoniae IgA1P has emerged as a promising antibacte

244 Thus, S. pneumoniae modulates mRNA and miR expression by lung

245 Thus, S. pneumoniae senses and responds to Neu5Ac, leading to

246 -binding residues, PspCNs from D39 and Tigr4 S. pneumoniae exhibit similar FH-anchoring and enhancing

247 pulmonary neutrophils, a level comparable to S. pneumoniae-challenged, conventionally fed young mice.

248 Mice exposed to S. pneumoniae prior to IAV do not maintain the initially

249 In mice exposed to S. pneumoniae prior to IAV, the initial virus-specific g

250 As immunity to S. pneumoniae infection is highly complement dependent,

251 he acute-phase protein C-reactive protein to S. pneumoniae, thereby reducing activation of the classi

252 the age-associated decline in resistance to S. pneumoniae, young (4 mo) and old (22-24 mo) C57BL/6 m

253 e enhanced early inflammation in response to S. pneumoniae and its lipoteichoic acid, demonstrate tha

254 endoplasmic reticulum stress in response to S. pneumoniae augmented inositol-requiring protein 1/X-b

255 iating neutrophil recruitment in response to S. pneumoniae infection.

256 e failed to increase hepcidin in response to S. pneumoniae or influenza infection and had greatly dim

257 ing the initiation of the immune response to S. pneumoniae to induce the subsequent production of PS-

258 In response to S. pneumoniae, dendritic cells and MyD88, an important a

259 ction, including type I IFNs, in response to S. pneumoniae.

260 sion of transcription factors in response to S. pneumoniae.

261 Reduced Th17 responses to S. pneumoniae in PBMCs of IP children can be rescued by

262 rminants of TLR-mediated immune responses to S. pneumoniae.

263 kinase-4-mediated inflammatory responses to S. pneumoniae.

264 The increased susceptibility to S. pneumoniae infection in Stat1(-/-) mice is also intri

265 ver, Stat1(-/-) mice are more susceptible to S. pneumoniae infection, which can be rescued by the ser

266 ol diet were exquisitely more susceptible to S. pneumoniae than young mice.

267 to why older persons are more susceptible to S. pneumoniae, and provide a possible mechanism to enhan

268 cus pneumoniae [including the unencapsulated S. pneumoniae, serotype 2 strain (R36A)] markedly inhibi

269 form of PLA2 (cPLA2alpha) was activated upon S. pneumoniae infection of cultured lung epithelial cell

270 d decreased cytokine production in vivo upon S. pneumoniae infection.

271 ive immune response against native CPS using S. pneumoniae serotype 5 (ST-5), a problematic CPS compo

272 oimmunization studies using cOVA and various S. pneumoniae mutants, each genetically deficient in one

273 e treatments with gemcitabine during in vivo S. pneumoniae infection decreased morbidity and mortalit

274 We sought to determine whether S. pneumoniae can (1) translocate the heart, (2) induce

275 These data explain the mechanisms by which S. pneumoniae colonize the human nasopharynx without ind

276 ion in the lung has been developed, in which S. pneumoniae persisted in the lungs for at least 28 day

277 While S. pneumoniae produces at least 94 antigenically differe

278 active Ags and TLR2 agonists associated with S. pneumoniae.

279 systemic infection after lung challenge with S. pneumoniae As phospholipase A2 (PLA2) promotes the re

280 tion upon high-dose pulmonary challenge with S. pneumoniae in vivo, thus implicating HXA3 in pneumoco

281 mice upon high-dose pulmonary challenge with S. pneumoniae The cPLA2alpha-deficient mice also suffere

282 llations of rIFN-gamma before challenge with S. pneumoniae.

283 Neonatal airway colonization with S. pneumoniae, H. influenzae, or M. catarrhalis is assoc

284 (+) T cells in response to immunization with S. pneumoniae expressing OVA peptide, did not inhibit T

285 of PFCE-O(2)-treated HbSS mice infected with S. pneumoniae is associated with altered pulmonary infla

286 6 (control) mice intravenously infected with S. pneumoniae were treated intravenously with PFCE or ph

287 In experiments with SCID mice infected with S. pneumoniae, we found passive transfer of IgG-depleted

288 sgenic sickle cell (HbSS) mice infected with S. pneumoniae.

289 c for 4 wk and intratracheally infected with S. pneumoniae.

290 Mice were intranasally infected with S. pneumoniae.

291 r 10 days before intravitreal infection with S. pneumoniae E353.

292 he protection of mice against infection with S. pneumoniae in which iNKT cells have previously been f

293 After infection with S. pneumoniae via the airways, dap12 mice demonstrated r

294 mechanisms during early lung infection with S. pneumoniae.

295 matory responses after airway infection with S. pneumoniae.

296 Lung neutrophils from mice with S. pneumoniae pneumonia contained 4127 DE mRNAs, 36% of

297 colonized the NPs of adult C57BL/6 mice with S. pneumoniae serotype (ST) 6A or 8 and then coinfected

298 s somewhat similar to the scenario seen with S. pneumoniae.

299 necrosis factor-alpha upon stimulation with S. pneumoniae and displayed increased phagocytosis of th

300 nfluenzae (mostly nontypeable) together with S. pneumoniae.