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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
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
27 spectra evaluation correctly identified all S. pneumoniae and S. pseudopneumoniae strains but miside
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
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
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
41 neuraminidase-expressing influenza virus and S. pneumoniae potentiates both colonization and infectio
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
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
54 ve transforming growth factor (TGF)-beta1 by S. pneumoniae in human host cells and highlight the key
56 xacerbates nasal colonization and disease by S. pneumoniae, in part via the synergistic contributions
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
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.
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
72 utrophils were indispensable for controlling S. pneumoniae outgrowth but contributed to alveolar barr
75 and mouse lungs were infected with different S. pneumoniae strains (D39, A66, R6x, H2O2/pneumolysin/L
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
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
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
87 on with a high-dose inoculum of encapsulated S. pneumoniae, alveolar macrophage-independent clearance
91 with pneumonia who had positive cultures for S. pneumoniae from January 1, 2000 to December 31, 2013.
93 f PAF signaling rendered Pce dispensable for S. pneumoniae persistence, reinforcing that this enzyme
96 d here confirm the importance of pilus I for S. pneumoniae pathogenesis and the potential use of anti
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
102 been identified as nonopsonic receptors for S. pneumoniae in the lung, we used scavenger receptor kn
104 es and also with potassium and thymidine for S. pneumoniae For all other variations, gepotidacin MIC
106 and coculture of these respective APCs from S. pneumoniae- or OVA-immunized mice with OVA-specific T
109 drate-binding module (CBM), originating from S. pneumoniae, with a synthetic B type 2 neoglycolipid,
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
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
120 tial role for neutrophil-derived IL-1beta in S. pneumoniae infection, and they elucidate the role of
122 ntified a c-di-AMP binding protein (CabP) in S. pneumoniae using c-di-AMP affinity chromatography.
124 upport for the hypothesis that competence in S. pneumoniae is regulated in response to the accumulate
126 nly a partial rethink of septum formation in S. pneumoniae, but consideration of the modes of PBP loc
128 major and possibly sole function of GreA in S. pneumoniae is to prevent formation of backtracked elo
130 ow that generation of a mutator phenotype in S. pneumoniae through deletions of mutX, hexA or hexB en
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
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
143 utcome with regard to prevention of invasive S. pneumoniae pathogenesis with a protein vaccine simila
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
150 e presence of interesting antibacterial [MIC(S. pneumoniae) approximately 1.2 muM] and anticancer [IC
152 actiae, S. dysgalactiae, S. equi, S. mutans, S. pneumoniae, S. suis and S. uberis, as well as represe
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
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
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
174 -induced oxidative stress was independent of S. pneumoniae-derived H2O2 and pneumolysin but depended
179 d whole-genome sequencing of 140 isolates of S. pneumoniae recovered from bloodstream infection (n =
181 quisition of the serotype 4 capsule locus of S. pneumoniae TIGR4, following induction of competence f
186 tudy, we used a model of low multiplicity of S. pneumoniae infection with HL-1 mouse cardiomyocytes t
189 as observed with regard to the prevention of S. pneumoniae bacteremia, and there was no difference in
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
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
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)
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
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
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
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
228 contractility; (2) the new observation that S. pneumoniae is capable of translocation into the myoca
230 orescence microscopy (IFM), we observed that S. pneumoniae replication within the heart preceded visu
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
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
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.
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
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-
265 ver, Stat1(-/-) mice are more susceptible to S. pneumoniae infection, which can be rescued by the ser
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
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
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
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
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
292 he protection of mice against infection with S. pneumoniae in which iNKT cells have previously been f
297 colonized the NPs of adult C57BL/6 mice with S. pneumoniae serotype (ST) 6A or 8 and then coinfected
299 necrosis factor-alpha upon stimulation with S. pneumoniae and displayed increased phagocytosis of th
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