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1                                              S. pneumoniae (98/458; 21.4%) and Mycobacterium tubercul
2                                              S. pneumoniae density was substantially higher in vaccin
3                                              S. pneumoniae established effective commensal colonizati
4                                              S. pneumoniae invades the myocardium and induces cardiac
5                                              S. pneumoniae isolates were serotyped and tested for ant
6                                              S. pneumoniae responds to exogenous fatty acids by suppr
7                                              S. pneumoniae strain JMG1 (DeltafakB3) was deficient in
8                                              S. pneumoniae that colonized the respiratory epithelium
9                                              S. pneumoniae was detected in the myocardium of all NHPs
10                                              S. pneumoniae was the most common bacterial pathogen, ac
11                                              S. pneumoniae was the most common pathogen detected (n =
12                                              S. pneumoniae-induced suppression of the P2Y(2)-mediated
13                                              S. pneumoniae-PR8 coinfection elicited a robust IL-17A r
14 ia coli isolates by MIC and 30 S. aureus, 15 S. pneumoniae, and 15 S. pyogenes isolates by disk diffu
15 pneumonia caused by both group 1 and group 2 S. pneumoniae strains.
16 uency and other associated phenotypes of 208 S. pneumoniae clinical isolates representing at least 30
17 (131/273) was N. meningitidis, 45% (123/273) S. pneumoniae, and 7% (19/273) H. influenzae.
18                      Whole genome data on 29 S. pneumoniae isolates identified related strains (<30 s
19 value identification identified correctly 46 S. pneumoniae and 4 S. pseudopneumoniae but misidentifie
20 onfirmed as N. meningitidis (n = 2433; 56%), S. pneumoniae (n = 1758; 40%), or H. influenzae (n = 180
21 istant sequence type 156 (ST156) serotype 9V S. pneumoniae in 3 respiratory patients that resulted in
22    In addition, the UAD-2 assay identified a S. pneumoniae serotype in 3.72% of nonbacteremic CAP cas
23                         Here, we show that a S. pneumoniae serotype 6B ST90 strain, which does not ca
24 hibited their antibacterial activity against S. pneumoniae but did not affect their ability to activa
25  all displayed bactericidal activity against S. pneumoniae, but only CCL26 and CCL28 retained high an
26 L1 and CXCL5, improves host defenses against S. pneumoniae.
27 tive effect of allergic inflammation against S. pneumoniae pathogenesis.
28 as the host response to AA protected against S. pneumoniae lung disease, the IL-6 deficiency abrogate
29 vide serotype-independent protection against S. pneumoniae.
30 efore a promising drug lead scaffold against S. pneumoniae infections that could be administered indi
31 uding Streptococcus pyogenes, S. agalactiae, S. pneumoniae, and S. equi.
32  spectra evaluation correctly identified all S. pneumoniae and S. pseudopneumoniae strains but miside
33 ults provide a correct identification of all S. pneumoniae and S. pseudopneumoniae isolates.
34 red by PAF and the bacterial cell wall allow S. pneumoniae to leverage a ChoP-remodeling enzyme (Pce)
35 d to the virulence of S. pneumoniae Although S. pneumoniae is known to use a sophisticated enzyme mac
36 e type 217 was the most common lineage among S. pneumoniae isolates.
37 studied histidine triad protein D (PhtD), an S. pneumoniae adhesin vaccine candidate, for its ability
38 del of secondary bacterial pneumonia with an S. pneumoniae strain that is innocuous to mice in the ab
39  Specific qPCR tests targeting S. aureus and S. pneumoniae did not provide additional diagnoses but p
40       The qPCR tests targeting S. aureus and S. pneumoniae gave earlier results than culture and panb
41 mice from septicemia caused by S. aureus and S. pneumoniae, whereas untreated mice die within 24-33 h
42 nt of the DeltaplsX strains of S. aureus and S. pneumoniae.
43 -17A response that promotes inflammation and S. pneumoniae disease in the nasopharynx.
44 m and pH 5.5 (no growth of H. influenzae and S. pneumoniae by BMD).
45 ainst nontypeable Haemophilus influenzae and S. pneumoniae, engendering protection against acute otit
46 e regulation of airway barrier integrity and S. pneumoniae disease.
47                   Neisseria meningitidis and S. pneumoniae remain important causes of meningitis in c
48 growth and viability in L. monocytogenes and S. pneumoniae.
49       However, neutrophil uptake of MRSA and S. pneumoniae was significantly reduced upon IFN-lambda
50 % CI = 1.29-4.88; n = 921 participants), and S. pneumoniae community-acquired pneumonia (OR = 2.15; 9
51 neuraminidase-expressing influenza virus and S. pneumoniae potentiates both colonization and infectio
52  interaction between respiratory viruses and S. pneumoniae in CAAP pathogenesis.
53 tic fluoroquinolone-resistant MRSA, VRE, and S. pneumoniae, and the possibility to offer patients an
54          Predominant causative pathogens are S. pneumoniae and H. influenzae.
55 th instigated by pore-forming toxins such as S. pneumoniae pneumolysin.
56 ocus of public health strategies directed at S. pneumoniae.
57 and behavioral changes, as well as attenuate S. pneumoniae infectivity.
58  or the immunochromatographic (ICT) BinaxNow S. pneumoniae test (composite diagnostic) was positive.
59 acological inhibition of this enzyme blocked S. pneumoniae-induced PMN transepithelial migration in v
60  intercepting the competence regulon in both S. pneumoniae specificity groups with activities at the
61 d functional changes in the biofilms of both S. pneumoniae and S. aureus.
62  2013-2015, and 2016-2018 in cases caused by S. pneumoniae (5.1% [15/294], 65.9% [58/88], and 52.1% [
63  of radiographically confirmed CAP caused by S. pneumoniae serotypes in hospitalized US adults.
64 xacerbates nasal colonization and disease by S. pneumoniae, in part via the synergistic contributions
65  and the most prevalent sugar encountered by S. pneumoniae during invasive disease.
66 ssion and middle ear inflammation induced by S. pneumoniae and reduced hearing loss and pneumococcal
67 thophysiology of oxidative stress induced by S. pneumoniae and the role of nuclear factor erythroid 2
68 ant induction of oxidative stress induced by S. pneumoniae in vivo, ex vivo, and in vitro.
69 with acute pneumonia, and H2O2 production by S. pneumoniae in vivo contributes to its genotoxicity an
70 tibodies against host proteins recognized by S. pneumoniae adhesins, we showed that S. pneumoniae upt
71 geal colonisation model, black carbon caused S. pneumoniae to spread from the nasopharynx to the lung
72 tion, and influenza virus coinfection caused S. pneumoniae NP density to increase, resulting in bacte
73  absence of Pce, neutrophils rapidly cleared S. pneumoniae from the airway and impeded invasive disea
74 The TAC method was evaluated on 146 clinical S. pneumoniae isolates and 13 nonpneumococcal species th
75 such as influenza A virus, induces commensal S. pneumoniae to disseminate beyond the nasopharynx and
76                                Consistently, S. pneumoniae D39 caused higher cytotoxicity to RAW 264.
77 utrophils were indispensable for controlling S. pneumoniae outgrowth but contributed to alveolar barr
78                 We show that a PLY-deficient S. pneumoniae mutant was impaired in triggering human ne
79 -specific IgGs in serum, the newly developed S. pneumoniae CPS microarrays offer the advantage of ena
80                                    Different S. pneumoniae strains caused distinct cardiac pathologie
81 arbon sources on CPS production in different S. pneumoniae serotypes may contribute to a better under
82 ng described in this study can differentiate S. pneumoniae from other Streptococcus species.
83 -off absorbance-value of 2.1, differentiated S. pneumoniae from all but one other mitis group strepto
84 uring both colonization and invasive disease S. pneumoniae ferments host-derived carbohydrates as its
85        During invasive pneumococcal disease, S. pneumoniae can gain access to the myocardium, kill ca
86 data demonstrate a key role for PAR-1 during S. pneumoniae lung infection that is mediated, at least
87 , we show that Il22ra2 inhibits IL-22 during S. pneumoniae lung infection and that Il22ra2 deficiency
88 of PLA2 in local and systemic disease during S. pneumoniae infection.
89 As (miRs) in lung neutrophils in mice during S. pneumoniae pneumonia and performed in depth in silico
90 on with a high-dose inoculum of encapsulated S. pneumoniae, alveolar macrophage-independent clearance
91 pid bacterial replication, with an estimated S. pneumoniae doubling time of 16 min.
92        Moreover, in the presence of ethanol, S. pneumoniae AdhE produced acetaldehyde and NADH, which
93 ired for lethal systemic infection following S. pneumoniae lung challenge.
94 injured mice had greater mortality following S. pneumoniae infection, which suggests that respiratory
95 with pneumonia who had positive cultures for S. pneumoniae from January 1, 2000 to December 31, 2013.
96                  Nasopharyngeal cultures for S. pneumoniae were obtained daily from children aged <5
97             Of 643 patients hospitalized for S. pneumoniae pneumonia, 139 (22%) were macrolide resist
98 d here confirm the importance of pilus I for S. pneumoniae pathogenesis and the potential use of anti
99                  Hence, LTA is important for S. pneumoniae to establish systemic infections, and TacL
100 aecalis ATCC 29212, 0.008 to 0.03 mug/ml for S. pneumoniae ATCC 49619, and 2 to 8 mug/ml for H. influ
101 mm for S. aureus ATCC 25923, 25 to 31 mm for S. pneumoniae ATCC 49619, and 16 to 20 mm for H. influen
102 oncentration (MIC) of RSM-932A and MN58b for S. pneumoniae was 0.4 muM and 10 muM, respectively, and
103 ): of 35 samples that were qPCR positive for S. pneumoniae, N. meningitidis, and H. influenzae, only
104                      A model is proposed for S. pneumoniae SczA function in which both A- and B-sites
105 in (91% sensitivity and 100% specificity for S. pneumoniae and 81% sensitivity and 100% specificity f
106 on (75% sensitivity and 100% specificity for S. pneumoniae) for clinical metagenomic sputum samples.
107 es and also with potassium and thymidine for S. pneumoniae For all other variations, gepotidacin MIC
108  and coculture of these respective APCs from S. pneumoniae- or OVA-immunized mice with OVA-specific T
109 w family 20 glycoside hydrolase, GH20C, from S. pneumoniae.
110 creased more than 2-fold in neutrophils from S. pneumoniae pneumonia.
111 drate-binding module (CBM), originating from S. pneumoniae, with a synthetic B type 2 neoglycolipid,
112 ultiple-antigen vaccines (MAV) prepared from S. pneumoniae TIGR4 lysates enriched for surface protein
113 vide immediate and essential protection from S. pneumoniae through production of natural Ig, which ha
114 nge of H(2)O(2) concentrations in vitro from S. pneumoniae, highlighting their potential for facile r
115 s caused by both homologous and heterologous S. pneumoniae strains.
116 ern because - in contrast to HRSV and HMPV - S. pneumoniae can become part of the nasopharyngeal flor
117 enotypic TaqMan array card (TAC) to identify S. pneumoniae strains, including lytA-based sequences, a
118 he A- and B-site SczA mutant variants impact S. pneumoniae resistance to zinc toxicity and survival i
119                                 Importantly, S. pneumoniae induces DSBs in the lungs of animals with
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  the mgtA gene encoding a PII-type ATPase in S. pneumoniae, suggested previously to function in Ca2+
123 atile surveyor of available carbohydrates in S. pneumoniae.
124  reverse-engineer gene expression control in S. pneumoniae A selection platform is described that all
125 egrated into the CCR regulatory framework in S. pneumoniae.
126 iptional characteristics of the cps locus in S. pneumoniae.
127 rtality rate, in contrast to no mortality in S. pneumoniae-infected sham (Sham + Sp) animals.
128                 We test these predictions in S. pneumoniae and find that the duration of carriage of
129            Zinc intoxication is prevented in S. pneumoniae by expression of the zinc exporter CzcD, w
130 PG synthesis, but do not control its rate in S. pneumoniae.
131 ism of failure of Th17 immunity resulting in S. pneumoniae infections in children <2 years old.
132                The expression of SPD_0247 in S. pneumoniae harvested from infected tissues was signif
133  is shown here through functional studies in S. pneumoniae that an unannotated homodimeric TetR from
134 ster than observed over longer timescales in S. pneumoniae and other bacteria drives high within-host
135 ing partner relative to FtsZ treadmilling in S. pneumoniae cells.
136 e against extracellular pathogens, including S. pneumoniae, we hypothesized that ethanol impairs muco
137                                      Indeed, S. pneumoniae invasion of HL-1 cells occurred through cl
138 ivative of the alkaloid vincamine, inhibited S. pneumoniae-induced mucin MUC5AC upregulation in cultu
139                       At 3 days post-injury, S. pneumoniae-infected traumatic brain injury mice (TBI
140 derived cells, depleted by CLs, internalized S. pneumoniae in vivo, whereas CD11c(low) dendritic cell
141                                Intriguingly, S. pneumoniae can utilize several plant oligosaccharides
142 d, the initial interactions of heart-invaded S. pneumoniae with cardiomyocytes remain unclear.
143 influenza strain, PR8, resulting in invasive S. pneumoniae disease.
144 utcome with regard to prevention of invasive S. pneumoniae pathogenesis with a protein vaccine simila
145 ndidate, for its ability to prevent invasive S. pneumoniae disease in adult and infant mice.
146 rrow neutrophils stimulated with heat-killed S. pneumoniae (signal 1) and pneumolysin (signal 2) exhi
147 s of IP children stimulated with heat-killed S. pneumoniae had significantly reduced percentages of C
148 dependent cytolysin (CDC) family, is a major S. pneumoniae virulence factor that generates ~25-nm dia
149 NA copies per LAMP zone for N. meningitidis, S. pneumoniae and Hib were achieved within 1h.
150 erage annual incidences for N. meningitidis, S. pneumoniae, and H. influenzae, respectively, were 7.5
151 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
153                             To mimic natural S. pneumoniae pathogenesis, we commensally colonized the
154 erstanding the epidemiology of nonbacteremic S. pneumoniae CAP and for assessing the efficacy of futu
155 ted to increased carriage of nonencapsulated S. pneumoniae (NESp).
156 tion, thereby enabling otherwise noninvasive S. pneumoniae to cause deadly pneumonia.
157           IRRs for single NTHi, mixed NTHi + S. pneumoniae, and all-NTHi OM were 0.30 (0.25-0.35), 0.
158 cillin resistance was found in 16% (4/25) of S. pneumoniae isolates.
159         PCV13 serotypes made up 88% (7/8) of S. pneumoniae meningitis prevaccination and 20% (5/20) p
160                     The enigmatic ability of S. pneumoniae to utilize RFOs has recently received atte
161 ly correlated with the relative abundance of S. pneumoniae.
162 nother tool that is unique in the arsenal of S. pneumoniae and that it may implement the effort of th
163 n stress, but only in genetic backgrounds of S. pneumoniae and Bacillus subtilis that exhibit Mn2+ se
164 cifically affecting the adhesive capacity of S. pneumoniae led to the identification of the monoclona
165 r understanding of the extensive capacity of S. pneumoniae to process host glycans and the likely rol
166 ment but did not influence total carriage of S. pneumoniae, H. influenzae, or S. aureus.
167                                 Clearance of S. pneumoniae from lungs of HbSS mice or C57BL/6 mice wa
168 hat CozE is a member of the MreCD complex of S. pneumoniae that directs the activity of PBP1a to the
169 ng inflammation during AA and the control of S. pneumoniae bacterial disease.
170 mples for the serotype-specific detection of S. pneumoniae Sputum optimization involved liquefaction
171 at qPCR significantly increases detection of S. pneumoniae, N. meningitidis, and H. influenzae in CSF
172 , direct, and serotype-specific detection of S. pneumoniae, which may improve postvaccination serotyp
173 p streptococci, including differentiation of S. pneumoniae from Streptococcus pseudopneumoniae.
174 roteins are involved in the encapsulation of S. pneumoniae in a posttranscriptional manner.
175 th cases and controls, with the exception of S. pneumoniae in exposed controls, which was detected 25
176 molysin (PLY) is a major virulence factor of S. pneumoniae and a target for both small molecule drug
177 ells via the release of bacterial factors of S. pneumoniae.
178                  Thus, the multiple FakBs of S. pneumoniae permit the utilization of the entire spect
179                                The impact of S. pneumoniae on host molecular processes that lead to d
180 -induced oxidative stress was independent of S. pneumoniae-derived H2O2 and pneumolysin but depended
181               The intracerebral injection of S. pneumoniae D39 induced the recruitment of B and T cel
182 nia was induced by intranasal inoculation of S. pneumoniae.
183  studied at 6 and 24 h after instillation of S. pneumoniae or PBS.
184 d whole-genome sequencing of 140 isolates of S. pneumoniae recovered from bloodstream infection (n =
185 le cocci, suggesting that only a minority of S. pneumoniae are poised to cross the BBB.
186                      Using a murine model of S. pneumoniae corneal infection, we demonstrated a requi
187               We have used a murine model of S. pneumoniae early lung infection with wild-type, unenc
188 tudy, we used a model of low multiplicity of S. pneumoniae infection with HL-1 mouse cardiomyocytes t
189 necroptosis inhibition reduced the number of S. pneumoniae foci observed in hearts of acutely infecte
190                The decline in the numbers of S. pneumoniae meningitis post-PCV13 is encouraging and s
191 e expression control on the pathogenicity of S. pneumoniae.
192  with implications in the pathophysiology of S. pneumoniae infection.
193 V also significantly reduced phagocytosis of S. pneumoniae by 33% in COPD MDM (n = 20; P = 0.0192).
194                   During the acute phases of S. pneumoniae infection, these populations of splenic ne
195 ed response is suppressed in the presence of S. pneumoniae in A549 and isolated primary alveolar cell
196 pre-PCV and post-PCV eras, the prevalence of S. pneumoniae bacteremia dropped across all age groups (
197 as observed with regard to the prevention of S. pneumoniae bacteremia, and there was no difference in
198  mediating the immunosuppressive property of S. pneumoniae.
199 n patients with pneumonia, the proportion of S. pneumoniae-specific plasmablasts expressing L-selecti
200 ion with PCV13 led to a greater reduction of S. pneumoniae NP density (>2.5 log units) than PhtD vacc
201 s, attesting to intracellular replication of S. pneumoniae as a key first step in pneumococcal pathog
202 an hydrolase CbpD that targets the septum of S. pneumoniae cells to show that class A PBPs have an au
203 ressure by human CMV and the 23F serotype of S. pneumoniae acted on the IGVK3-11 and IGVH3-30 genes a
204 o both an invasive and noninvasive strain of S. pneumoniae (D39 and EF3030) but that PAR-1 antagonism
205 , we compared an isogenic deletion strain of S. pneumoniae TIGR4 in polyamine transport operon (Delta
206       Homologous and heterologous strains of S. pneumoniae were opsonized after incubation in sera fr
207 wofold higher expression compared to that of S. pneumoniae R6, could also confer increased resistance
208 development of therapeutics for treatment of S. pneumoniae.
209 y that is tightly linked to the virulence of S. pneumoniae Although S. pneumoniae is known to use a s
210 tic activity, colonization, and virulence of S. pneumoniae, as well as host cell myeloperoxidase acti
211 inst the capsular polysaccharide (CPS) offer S. pneumoniae serotype-specific protection.
212 opsonic capacity by increasing C3 binding on S. pneumoniae Taken together, endogenous IL-22 and hepat
213 n, and cutaneous lymphocyte antigen (CLA) on S. pneumoniae-specific plasmablasts was examined in pati
214 increased C4b and reduced C4dg deposition on S. pneumoniae D39.
215 lide use and PCV7 and PCV13 introductions on S. pneumoniae were associated with changes in macrolide
216 nd whole genome sequencing were performed on S. pneumoniae isolates.
217 t in one of the CBPs, demonstrated that only S. pneumoniae lacking the CBP pneumococcal surface prote
218 dens upon superinfection with either MRSA or S. pneumoniae Surprisingly, adhesion molecule expression
219 s after intratracheal instillation of PBS or S. pneumoniae, and differentially expressed (DE) mRNAs a
220                                     Overall, S. pneumoniae (53.4%), Neisseria meningitidis (13.7%), a
221 (N. meningitidis), Streptococcus pneumoniae (S. pneumoniae), and Haemophilus influenzae type b (Hib)
222 eus (S. aureus) or Streptococcus pneumoniae (S. pneumoniae), respectively; and a qPCR assay targeting
223  with positive UAT more often had a positive S. pneumoniae culture (25.4% vs. 1.9%, p<0.001) and less
224 uenza virus on the surface of Gram-positive, S. pneumoniae and S. aureus, and Gram-negative, Moraxell
225 g the importance of DNA repair in preventing S. pneumoniae-induced genotoxicity.
226  using a collection of 22 microarray-printed S. pneumoniae CPSs.
227 s suppressed the IL-17A response and reduced S. pneumoniae invasion in RAG1-/- mice.
228           RoRgammat-/- mice also had reduced S. pneumoniae disease in a coinfection model.
229 e nasopharynx; IL-17A neutralization reduced S. pneumoniae invasive disease.
230   Our data show that although IL-17A reduces S. pneumoniae colonization, coinfection with influenza v
231 atients hospitalized for macrolide-resistant S. pneumoniae pneumonia were more severely ill on presen
232 riments with the sensitive laboratory strain S. pneumoniae R6 as recipient.
233 e regulon can therefore be utilized to study S. pneumoniae cell-cell communication and behavioral cha
234 populations and MZ B cells regulate systemic S. pneumoniae clearance through complementary mechanisms
235                                The fact that S. pneumoniae, H. influenzae, and S. aureus polymicrobia
236 of evolutionary theory, we hypothesized that S. pneumoniae use owner-intruder asymmetries to settle c
237  contractility; (2) the new observation that S. pneumoniae is capable of translocation into the myoca
238                             We observed that S. pneumoniae mutants deficient in NanA and beta-galacto
239 orescence microscopy (IFM), we observed that S. pneumoniae replication within the heart preceded visu
240 pinning-disk live-cell imaging revealed that S. pneumoniae induces P2Y(2) translocation into the cyto
241 umococcal carriage model (EHPC) to show that S. pneumoniae colonisation is associated with epithelial
242         In conclusion, our results show that S. pneumoniae directly inhibits purinergic signaling by
243                           Here, we show that S. pneumoniae induces toxic DNA double-strand breaks (DS
244 smission electron microscopy, we showed that S. pneumoniae rapidly adhered to and invaded cardiomyocy
245 ed by S. pneumoniae adhesins, we showed that S. pneumoniae uptake by cardiomyocytes is not through th
246                We have previously shown that S. pneumoniae infection of the respiratory epithelium in
247        Taken together, this study shows that S. pneumoniae-induced damage to the host cell genome exa
248 al doubling time increased to 56 min and the S. pneumoniae alveolar macrophage-dependent clearance ha
249 We first described a UAD assay to detect the S. pneumoniae serotypes 1, 3, 4, 5, 6A, 6B, 7F, 9V, 14,
250 r haptenic component of teichoic acid in the S. pneumoniae cell wall, and lipoteichoic acid in the S.
251 niae cell wall, and lipoteichoic acid in the S. pneumoniae membrane were previously reported to be im
252 eptococcus pneumoniae Some components of the S. pneumoniae glycoconjugate vaccine Prevnar13 that cont
253 ors in developing more refined models of the S. pneumoniae-host interaction.
254                     Here, we showed that the S. pneumoniae type 2 D39 strain is ethanol tolerant and
255    In addition, our results suggest that the S. pneumoniae yybP-ykoY riboswitch functions to regulate
256                                        Thus, S. pneumoniae modulates mRNA and miR expression by lung
257                                        Thus, S. pneumoniae senses and responds to Neu5Ac, leading to
258 -binding residues, PspCNs from D39 and Tigr4 S. pneumoniae exhibit similar FH-anchoring and enhancing
259 pulmonary neutrophils, a level comparable to S. pneumoniae-challenged, conventionally fed young mice.
260 ht on the susceptibility of older persons to S. pneumoniae and provide a possible therapeutic to impr
261 he acute-phase protein C-reactive protein to S. pneumoniae, thereby reducing activation of the classi
262 mechanism behind this interaction related to S. pneumoniae respiratory illnesses.
263  the age-associated decline in resistance to S. pneumoniae, young (4 mo) and old (22-24 mo) C57BL/6 m
264      Il22ra2(-/-) mice are more resistant to S. pneumoniae infection, have increased IL-22 in lung ti
265 iating neutrophil recruitment in response to S. pneumoniae infection.
266 sion of transcription factors in response to S. pneumoniae.
267 ed adult macrophages and lung in response to S. pneumoniae.
268                    Reduced Th17 responses to S. pneumoniae in PBMCs of IP children can be rescued by
269              The increased susceptibility to S. pneumoniae infection in Stat1(-/-) mice is also intri
270 ver, Stat1(-/-) mice are more susceptible to S. pneumoniae infection, which can be rescued by the ser
271 ol diet were exquisitely more susceptible to S. pneumoniae than young mice.
272 cus pneumoniae [including the unencapsulated S. pneumoniae, serotype 2 strain (R36A)] markedly inhibi
273 form of PLA2 (cPLA2alpha) was activated upon S. pneumoniae infection of cultured lung epithelial cell
274 ive immune response against native CPS using S. pneumoniae serotype 5 (ST-5), a problematic CPS compo
275 of within-host competitive success utilizing S. pneumoniae colonization of the upper respiratory trac
276 , and 23F, covered by the licensed 13-valent S. pneumoniae conjugate vaccine.
277 oimmunization studies using cOVA and various S. pneumoniae mutants, each genetically deficient in one
278                                         When S. pneumoniae D39 was opsonized with human serum, the la
279 ce of the capsular polysaccharide (CPS) when S. pneumoniae was grown on fructose.
280 cus aureus has two binding proteins, whereas S. pneumoniae expresses three.
281               We sought to determine whether S. pneumoniae can (1) translocate the heart, (2) induce
282                                        While S. pneumoniae produces at least 94 antigenically differe
283 systemic infection after lung challenge with S. pneumoniae As phospholipase A2 (PLA2) promotes the re
284 mice upon high-dose pulmonary challenge with S. pneumoniae The cPLA2alpha-deficient mice also suffere
285 n-rescued mice 3 months after challenge with S. pneumoniae.
286 logical consolidation or pleural fluid, with S. pneumoniae and S. aureus the leading pathogens identi
287 (+) T cells in response to immunization with S. pneumoniae expressing OVA peptide, did not inhibit T
288 6 (control) mice intravenously infected with S. pneumoniae were treated intravenously with PFCE or ph
289  In experiments with SCID mice infected with S. pneumoniae, we found passive transfer of IgG-depleted
290 sgenic sickle cell (HbSS) mice infected with S. pneumoniae.
291 c for 4 wk and intratracheally infected with S. pneumoniae.
292 r 10 days before intravitreal infection with S. pneumoniae E353.
293 he protection of mice against infection with S. pneumoniae in which iNKT cells have previously been f
294 d OXPHOS gene expression upon infection with S. pneumoniae, changes that were IL-22 dependent.
295                          Upon infection with S. pneumoniae, Spp1(+/+) mice with allergic airway infla
296  mechanisms during early lung infection with S. pneumoniae.
297 7BL/6 mice were intranasally inoculated with S. pneumoniae serotype 6A to establish colonization and
298 rtical impact and infected intranasally with S. pneumoniae (1,500 colony-forming units) or vehicle (p
299              Lung neutrophils from mice with S. pneumoniae pneumonia contained 4127 DE mRNAs, 36% of
300 colonized the NPs of adult C57BL/6 mice with S. pneumoniae serotype (ST) 6A or 8 and then coinfected

 
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