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1 sufficiency with increased susceptibility to pneumococcal infection.
2 play important roles in host defense against pneumococcal infection.
3  they may be involved at different stages of pneumococcal infection.
4 s neuraminidase (NA) has in priming mice for pneumococcal infection.
5 peutic tool to protect against ALI caused by pneumococcal infection.
6 n-deficient mice were extremely sensitive to pneumococcal infection.
7 trepto-coccus pneumoniae and its role during pneumococcal infection.
8 fort to explore mucosal immunization against pneumococcal infection.
9 y to pneumolysin provides protection against pneumococcal infection.
10 e in adult mice and protect mice from lethal pneumococcal infection.
11 man antibody to PspA could protect mice from pneumococcal infection.
12  to provide optimal protection from virulent pneumococcal infection.
13 ed the role of CD40L in host defense against pneumococcal infection.
14 sodes of otitis media, and 116 deaths due to pneumococcal infection.
15 d do not protect against death from virulent pneumococcal infection.
16 BEAS-2B cell line for studying mechanisms of pneumococcal infection.
17 d elicit protective immune responses against pneumococcal infection.
18 can elicit protective immunity against fatal pneumococcal infection.
19 and the resulting protection of mice against pneumococcal infection.
20 CD) patients are at high risk of contracting pneumococcal infection.
21 astin (LPL) succumb rapidly to intratracheal pneumococcal infection.
22  this cell type in the immediate response to pneumococcal infection.
23  mutant CRP did not protect mice from lethal pneumococcal infection.
24 lly promotes a high risk of lethal, invasive pneumococcal infection.
25 ed initial protection of mice against lethal pneumococcal infection.
26 ar recruitment and bacterial loads following pneumococcal infection.
27 rways via this integrin at an early stage of pneumococcal infection.
28  genetic risk factors with predisposition to pneumococcal infection.
29 on within lung tissue, but for combating the pneumococcal infection.
30 ciated with differences in susceptibility to pneumococcal infection.
31  eliciting cross-protection immunity against pneumococcal infection.
32  of choice for patients with possible severe pneumococcal infection.
33 n vivo to reduced mouse morbidity from fatal pneumococcal infection.
34 e would become more susceptible to secondary pneumococcal infection.
35 tosis and rescues mice from life-threatening pneumococcal infection.
36 s of natural IgM-mediated protection against pneumococcal infection.
37  induce a protective immune response against pneumococcal infection.
38 and systemic immunity for protection against pneumococcal infection.
39 accination might be the key to prevention of pneumococcal infection.
40 nd may provide a novel target for preventing pneumococcal infection.
41 riants, each playing a different role during pneumococcal infection.
42 low CD4(+) cell counts have a higher rate of pneumococcal infection.
43 s a key molecule in the host defense against pneumococcal infection.
44 ty, improving clinical outcomes after severe pneumococcal infection.
45 at T cell immunity may be protective against pneumococcal infection.
46 he efficacy of beta-lactams for treatment of pneumococcal infection.
47 ell wall and provides innate defense against pneumococcal infection.
48 en implicated in increased susceptibility to pneumococcal infection.
49  the effectiveness of existing therapies for pneumococcal infections.
50 s part of the protein are protective against pneumococcal infections.
51 nd in populations with a higher incidence of pneumococcal infections.
52 moking and other factors as risk factors for pneumococcal infections.
53 y of a MAb to passively protect mice against pneumococcal infections.
54 ed, which determined the clinical outcome of pneumococcal infections.
55 ers to intravenous (i.v.) penicillin use for pneumococcal infections.
56 ine antigen test in patients with bacteremic pneumococcal infections.
57 ermine what proportion could be confirmed as pneumococcal infections.
58 -infected patients have an increased rate of pneumococcal infections.
59 es now represent the best strategy to combat pneumococcal infections.
60 ne candidate for protection against invasive pneumococcal infections.
61 e inflammatory profiles are generated during pneumococcal infection, a common pattern emerged, which
62                                              Pneumococcal infections account for a significant propor
63 ent of, and outcomes in, septic shock during pneumococcal infection, acute respiratory distress syndr
64 ction of the protective humoral responses to pneumococcal infection, administration of MR-1 had no ef
65      Stimulation of CCL2 by macrophages upon pneumococcal infection alone required the pattern recogn
66                 To identify risk factors for pneumococcal infection among human immunodeficiency viru
67  intravenous, and intranasal routes prior to pneumococcal infection and by aerosol 24 h following inf
68 o role of AM MARCO in innate defense against pneumococcal infection and environmental particles.
69 lay an important role in the pathogenesis of pneumococcal infection and has been identified as a puta
70 S61F is an effective mucosal vaccine against pneumococcal infection and induces CD4+ Th2-type cells,
71 e in eliciting pulmonary inflammation during pneumococcal infection and is required for lethal system
72 that cigarette smoke predisposes to invasive pneumococcal infection and mortality in an animal model.
73 is indispensable for innate immunity against pneumococcal infection and that PspA interferes with the
74 f macrophage deactivation for the outcome of pneumococcal infections and highlight the role of LCN2 a
75 t has been shown that CRP protects mice from pneumococcal infection, and an active complement system
76  Cirrhosis is a major risk factor for severe pneumococcal infection, and patients evaluated for liver
77  apoptosis of a variety of brain cells after pneumococcal infection arises from inhibition of PtdCho
78 ndeed, DNA was present in the cytosol during pneumococcal infection as indicated by the activation of
79 ects, this establishes a niche for secondary pneumococcal infection by altering early cellular innate
80 a major contribution in the host response to pneumococcal infection by increasing circulating neutrop
81 /c nor CBA/N mice were protected from lethal pneumococcal infections by immunization with peptide 1-B
82 one macrophages to protect against a primary pneumococcal infection can, under conditions of splenome
83 protected HIV-infected adults from recurrent pneumococcal infection caused by vaccine serotypes or se
84 e primary end point was a further episode of pneumococcal infection caused by vaccine serotypes or se
85   Serum from a patient recovering from acute pneumococcal infection contained IgG antibodies specific
86    The rate of antibiotic-resistant invasive pneumococcal infections decreased in young children and
87 her the frequency and character of secondary pneumococcal infections differed depending on the strain
88 the innate immune defense mechanisms against pneumococcal infection during the early stage of acute O
89 of antimicrobial agents for the treatment of pneumococcal infections for specific types of infection
90 varicella, and risk of invasive disease from pneumococcal infections have declined.
91 ke daily prophylactic antibiotics to prevent pneumococcal infections; however, how much prophylactic
92                    We used a database of all pneumococcal infections identified at our medical center
93                     Repeated observations of pneumococcal infection in 121 United Kingdom families (O
94  well as THP-1 macrophages produced MIF upon pneumococcal infection in a pneumolysin-dependent manner
95 in epidemiological investigation of invasive pneumococcal infection in adults, particularly if combin
96  generally considered a rare complication of pneumococcal infection in adults.
97 ding protein were increased (P < 0.05) after pneumococcal infection in both acutely ill and convalesc
98 e present study, we compared the severity of pneumococcal infection in C57BL/6 (B6) and 129Sv mice.
99 nia, which is a more common manifestation of pneumococcal infection in elderly persons.
100 uation and for determining the prevalence of pneumococcal infection in epidemiological studies of com
101 ctor capable of eliciting protection against pneumococcal infection in mice.
102 ining the increased vulnerability to acquire pneumococcal infection in parallel with sustained allerg
103 at there is a significant long-term risk for pneumococcal infection in patients who have undergone al
104  statin therapy might improve the outcome of pneumococcal infection in SCD.
105  an important role in hypersusceptibility to pneumococcal infection in sickle cell disease.
106 IL-22 was rapidly induced in the lung during pneumococcal infection in wild-type mice, and Il22(-/-)
107 d test for the early diagnosis of bacteremic pneumococcal infections in adult patients, even after an
108 aphic assay, for the diagnosis of bacteremic pneumococcal infections in hospitalized adult patients.
109 es to PspA may have some utility in treating pneumococcal infections in humans.
110 sible for almost 40% of penicillin-resistant pneumococcal infections in the United States in the late
111 ule is effective for preventing vaccine-type pneumococcal infections in young children not infected w
112 at treatment with exogenous sialic acid post-pneumococcal infection increased the numbers of CFU reco
113                                     Invasive pneumococcal infection (IPI) is the most common serious
114                                     Although pneumococcal infection is a serious problem worldwide an
115 at the extent of protection against systemic pneumococcal infection is influenced by target antigen a
116                      The diagnosis of severe pneumococcal infections is inadequate, relying heavily o
117 uction during concurrent influenza virus and pneumococcal infection leads to increased bacterial colo
118 mechanisms whereby pIgA may serve to control pneumococcal infections locally and upon the pathogen's
119 ity that cardiac scar formation after severe pneumococcal infection may explain why individuals who a
120 vaccination for protection against secondary pneumococcal infection, mice were immunized with pneumoc
121 ogens, whereas seasonality of other invasive pneumococcal infections might be primarily driven by inc
122                In order to monitor long-term pneumococcal infections noninvasively in living mice, a
123  role of microRNAs (miRNAs) as regulators in pneumococcal infection of human macrophages.
124 pe were found to have significant effects on pneumococcal infection of the nasopharynx, trachea, and
125                                              Pneumococcal infection of the respiratory tract is often
126 f asthma on the subsequent susceptibility to pneumococcal infection, ovalbumin (OVA)-induced allergic
127  of vaccine efficacy after dose 3 leading to pneumococcal infection), PCV13 and PPSV23 (Guillain-Barr
128 ear to have been selected for in vivo during pneumococcal infection, perhaps as a consequence of immu
129 ve inadequate antibiotic prophylaxis against pneumococcal infections, placing them at increased risk
130                 Finally, in a mouse model of pneumococcal infection, pneumolysin-producing pneumococc
131 itive rechallenges, and 34 cases of invasive pneumococcal infections possibly representing vaccine fa
132                                              Pneumococcal infections remain a leading cause of death
133                                              Pneumococcal infections remain the most important cause
134 other than the V1 H chain to protect against pneumococcal infection remains controversial.
135  to a 400-fold greater incidence of invasive pneumococcal infection resulting in fulminant, lethal pn
136 es and failed to effectively clear pulmonary pneumococcal infection, showing that immunodeficiency re
137                   HbSS mice developed severe pneumococcal infection significantly faster than C57BL/6
138 fer non-serotype-specific protection against pneumococcal infections such as pneumonia, meningitis, a
139 ith littermate controls after intrapulmonary pneumococcal infection, suggesting that IL-22 signaling
140 9Sv mice were remarkably more susceptible to pneumococcal infection than B6 mice.
141 nnate immune recognition pathway that senses pneumococcal infection, triggers type I IFN production,
142 ore, they should be partly protected against pneumococcal infection until month 15.
143 like receptor 4 (TLR4) confers resistance to pneumococcal infection via its interaction with pneumoly
144 , pulmonary innate defense against secondary pneumococcal infection was severely suppressed.
145 though a substantial proportion of recurrent pneumococcal infections was potentially preventable by v
146 er DAS181 would lead to an increased risk of pneumococcal infection, we tested S. pneumoniae coloniza
147          Risk profiles and manifestations of pneumococcal infection were ascertained from diagnosis,
148 er 1998, 14.9% (404/2717) of those who had a pneumococcal infection were HIV infected.
149 d control patients with penicillin-sensitive pneumococcal infections were compared.
150 eads to enhanced susceptibility to secondary pneumococcal infection, which can be prevented by IFN-ga
151 e phagocytosis during innate defense against pneumococcal infection, which may explain the associatio
152 tanding of molecular and cellular biology of pneumococcal infection will allow the development of new
153 usion protein was broadly protective against pneumococcal infection, with the potential for additiona

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