scholarly journals Streptococcus pneumoniae Endopeptidase O Promotes the Clearance of Staphylococcus aureus and Streptococcus pneumoniae via SH2 Domain-Containing Inositol Phosphatase 1-Mediated Complement Receptor 3 Upregulation

2020 ◽  
Vol 10 ◽  
Author(s):  
Sijie Li ◽  
Hong Zhang ◽  
Jiangming Xiao ◽  
Taixian Yuan ◽  
Zhaoche Shu ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Sh2 Domain ◽  
Complement Receptor ◽  
Inositol Phosphatase ◽  
Complement Receptor 3

Modulation of neutrophil complement receptor 3 expression by pneumococci

2003 ◽  
Vol 104 (6) ◽  
pp. 615-625 ◽  
Author(s):  
James H. WILLIAMS ◽  
Madeleine V. PAHL ◽  
Donna KWONG ◽  
Jeng ZHANG ◽  
Denise HATAKEYAMA ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
Fluorescence Microscopy ◽  
Morphological Changes ◽  
Surface Expression ◽  
Positive Control ◽  
Confocal Fluorescence Microscopy ◽  
Complement Receptor ◽  
Confocal Fluorescence ◽  
Complement Receptor 3 ◽  
Cell Counter

Complement receptor 3 (CR3; CD18/CD11b) plays an important role in the recognition and clearance of Streptococcus pneumoniae (pneumococci) by neutrophils. The purpose of the present study was to characterize the modulation of CR3 surface expression on neutrophils exposed to pneumococci and to assess its functional significance. CR3 was detected with fluorescent phytoerythrin-labelled anti-CR3 (CD11b) antibodies, quantified with a fluorescence cell counter (FACS) and localized by confocal fluorescence microscopy. Uptake of fluorescent FITC-labelled pneumococci was quantified by FACS. Whole blood from healthy volunteers was exposed at 37 °C to killed whole type III Streptococcus pneumoniae (KSP; 108/ml) or to a positive control (Escherichia coli lipopolysaccharide) that enhanced CR3 surface expression on neutrophils to a comparable extent. Varying the concentration of KSP between 105 and 108 organisms/ml progressively augmented CR3 surface expression measured at 1 h, whereas the response declined at 109/ml. The diminished response to 109 KSP/ml proved to be time-dependent, with surface CR3 up-regulated maximally within 5 min, and down-regulated thereafter. Labelling of CR3 during exposure demonstrated accelerated receptor sequestration, and confocal fluorescence microscopy demonstrated internalized CR3. Cooling to 16 °C, to inhibit the up-regulation of CR3 surface expression, also inhibited the uptake of FITC-labelled KSP and morphological changes. Accelerated down-regulation of surface CR3 expression by exposure to 109/ml unlabelled KSP diminished the uptake of labelled KSP added subsequently. In contrast, lipopolysaccharide-induced up-regulation of CR3 expression increased the uptake of labelled KSP. Together, these experiments reveal dynamic modulation of CR3 expression on the surface of neutrophils exposed to pneumococci and a functional correlate of this modulation. Thus neutrophil expression of CR3 changes dynamically in response to exposure of neutrophils to progressively higher concentrations of pneumococci, conditions that mimic early neutrophil recruitment to densely infected lung tissue in acute pneumococcal pneumonia.

scholarly journals Complement Receptor 3 Contributes to the Sexual Dimorphism in Neutrophil Killing of Staphylococcus aureus

2020 ◽  
Vol 205 (6) ◽  
pp. 1593-1600
Author(s):  
Srijana Pokhrel ◽  
Kathleen D. Triplett ◽  
Seth M. Daly ◽  
Jason A. Joyner ◽  
Geetanjali Sharma ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Sexual Dimorphism ◽  
Complement Receptor ◽  
Complement Receptor 3

Regulation of FcγR-stimulated phagocytosis by the 72-kDa inositol polyphosphate 5-phosphatase: SHIP1, but not the 72-kDa 5-phosphatase, regulates complement receptor 3–mediated phagocytosis by differential recruitment of these 5-phosphatases to the phagocytic cup

Blood ◽  
2007 ◽  
Vol 110 (13) ◽  
pp. 4480-4491 ◽  
Author(s):  
Kristy A. Horan ◽  
Ken-ichi Watanabe ◽  
Anne M. Kong ◽  
Charles G. Bailey ◽  
John E. J. Rasko ◽  
...  
Keyword(s):  
Time Lapse ◽  
Sh2 Domain ◽  
Dominant Negative ◽  
Complement Receptor ◽  
Inositol Polyphosphate ◽  
Src Homology ◽  
Complement Receptor 3 ◽  
Phagocytic Cups ◽  
Phosphoinositide 3 Kinase ◽  
Interfering Rna

Macrophages phagocytose particles to resolve infections and remove apoptotic cells. Phosphoinositide 3-kinase generates phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P3] is restricted to the phagocytic cup, promoting phagocytosis. The PtdIns(3,4,5)P3 5-phosphatase (5-ptase) Src homology 2 (SH2) domain-containing inositol-5-phosphatase 1 (SHIP1) inhibits phagocytosis. We report here that another PtdIns(3,4,5)P3-5-ptase, the 72-kDa-5-phosphatase (72-5ptase), inhibits Fcγ receptor (FcγR)– but not complement receptor 3 (CR3)–mediated phagocytosis, affecting pseudopod extension and phagosome closure. In contrast, SHIP1 inhibited FcγR and CR3 phagocytosis with greater effects on CR3-stimulated phagocytosis. The 72-5ptase and SHIP1 were both dynamically recruited to FcγR-stimulated phagocytic cups, but only SHIP1 was recruited to CR3-stimulated phagocytic cups. To determine whether 5-ptases focally degrade PtdIns(3,4,5)P3 at the phagocytic cup after specific stimuli, time-lapse imaging of specific biosensors was performed. Transfection of dominant-negative 72-5ptase or 72-5ptase small interfering RNA (siRNA) resulted in amplified and prolonged PtdIns(3,4,5)P3 at the phagocytic cup in response to FcγR- but not CR3-stimulation. In contrast, macrophages from Ship1−/−/AktPH-GFP transgenic mice exhibited increased and sustained PtdIns(3,4,5)P3 at the cup in response to CR3 activation, with minimal changes to FcγR activation. Therefore, 72-5ptase and SHIP1 exhibit specificity in regulating FcγR- versus CR3-stimulated phagocytosis by controlling the amplitude and duration of PtdIns(3,4,5)P3 at the phagocytic cup.

scholarly journals Antibiotic Susceptibility of Staphylococcus aureus and Streptococcus pneumoniae Isolates from the Nasopharynx of Febrile Children under 5 Years in Nanoro, Burkina Faso

Antibiotics ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 444
Author(s):  
Massa dit Achille Bonko ◽  
Palpouguini Lompo ◽  
Marc Christian Tahita ◽  
Francois Kiemde ◽  
Ibrahima Karama ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Burkina Faso ◽  
Antibiotic Susceptibility ◽  
Bacterial Colonization ◽  
Resistance To Penicillin ◽  
Tract Infections ◽  
Resistance Rates ◽  
Moderately Resistant ◽  
Children Under 5

(1) Background: nasopharynx colonization by resistant Staphylococcus aureus and Streptococcus pneumoniae can lead to serious diseases. Emerging resistance to antibiotics commonly used to treat infections due to these pathogens poses a serious threat to the health system. The present study aimed to determine the antibiotic susceptibility of S. aureus and S. pneumoniae isolates from the febrile children’s nasopharynx under 5 years in Nanoro (Burkina Faso). (2) Methods: bacterial isolates were identified from nasopharyngeal swabs prospectively collected from 629 febrile children. Antibiotic susceptibility of S. aureus and S. pneumoniae isolates was assessed by Kirby–Bauer method and results were interpreted according to the Clinical and Laboratory Standard Institute guidelines. (3) Results: bacterial colonization was confirmed in 154 (24.5%) of children of whom 96.1% carried S. aureus, 3.2% had S. pneumoniae, and 0.6% carried both bacteria. S. aureus isolates showed alarming resistance to penicillin (96.0%) and S. pneumoniae was highly resistant to tetracycline (100%) and trimethoprim–sulfamethoxazole (83.3%), and moderately resistant to penicillin (50.0%). Furthermore, 4.0% of S. aureus identified were methicillin resistant. (4) Conclusion: this study showed concerning resistance rates to antibiotics to treat suspected bacterial respiratory tract infections. The work highlights the necessity to implement continuous antibiotic resistance surveillance.

Pleural Fluid PCR Method for Detection of Staphylococcus aureus, Streptococcus pneumoniae and Haemophilus influenzae in Pediatric Parapneumonic Effusions

Respiration ◽  
2007 ◽  
Vol 75 (4) ◽  
pp. 437-442 ◽  
Author(s):  
G. Eda Utine ◽  
Ahmet Pinar ◽  
Uğur Özçelik ◽  
Burçin Şener ◽  
Ebru Yalçin ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Haemophilus Influenzae ◽  
Pleural Fluid ◽  
Pcr Method

scholarly journals β-Glucan enhances complement-mediated hematopoietic recovery after bone marrow injury

Blood ◽  
2006 ◽  
Vol 107 (2) ◽  
pp. 835-840 ◽  
Author(s):  
Daniel E. Cramer ◽  
Daniel J. Allendorf ◽  
Jarek T. Baran ◽  
Richard Hansen ◽  
Jose Marroquin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Serum ◽  
Complement Receptor ◽  
Dependent Manner ◽  
Complement Receptor 3 ◽  
Total Body ◽  
Stimulating Factor ◽  
Sublethal Irradiation ◽  
Classic Pathway

AbstractMyelotoxic injury in the bone marrow (BM) as a consequence of total body irradiation (TBI) or granulocyte colony-stimulating factor (G-CSF) mobilization results in the deposition of iC3b on BM stroma (stroma-iC3b). In the present study, we have examined how stroma-iC3b interacts with hematopoietic progenitor cells (HPCs) and the role of complement (C) and complement receptor 3 (CR3) in BM injury/repair. We demonstrate here that stroma-iC3b tethers HPCs via the inserted (I) domain of HPC complement receptor 3 (CR3, CD11b/CD18, Mac-1). Following irradiation, stroma-iC3b was observed in the presence of purified IgM and normal mouse serum (NMS), but not serum from Rag-2-/- mice, implicating a role for antibody (Ab) and the classic pathway of C activation. Furthermore, a novel role for soluble yeast β-glucan, a ligand for the CR3 lectin-like domain (LLD), in the priming of CR3+ HPC is suggested. Soluble yeast β-glucan could enhance the proliferation of tethered HPCs, promote leukocyte recovery following sublethal irradiation, and increase the survival of lethally irradiated animals following allogeneic HPC transplantation in a CR3-dependent manner. Taken together, these observations suggest a novel role for C, CR3, and β-glucan in the restoration of hematopoiesis following injury. (Blood. 2006;107:835-840)

scholarly journals In Vitro and In Vivo Activities of DA-7867, a New Oxazolidinone, against Aerobic Gram-Positive Bacteria

2005 ◽  
Vol 49 (6) ◽  
pp. 2498-2500 ◽  
Author(s):  
Eun Jeong Yoon ◽  
Yeong Woo Jo ◽  
Sung Hak Choi ◽  
Tae Ho Lee ◽  
Jae Keol Rhee ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Gram Positive ◽  
Methicillin Resistant ◽  
Gram Positive Bacteria ◽  
Vancomycin Resistant Enterococci ◽  
Infection Models ◽  
Vancomycin Resistant

ABSTRACT In vitro and in vivo activities of DA-7867 were assessed against methicillin-resistant Staphylococcus aureus, vancomycin-resistant enterococci, and penicillin-resistant Streptococcus pneumoniae. All isolates were inhibited by DA-7867 at ≤0.78 μg/ml, a four-times-lower concentration than that of inhibition by linezolid. For murine infection models, DA-7867 also exhibited greater efficacy than linezolid against all isolates tested.

scholarly journals Ceftaroline Activity against Bacterial Pathogens Frequently Isolated in U.S. Medical Centers: Results from Five Years of the AWARE Surveillance Program

2015 ◽  
Vol 59 (4) ◽  
pp. 2458-2461 ◽  
Author(s):  
Helio S. Sader ◽  
Robert K. Flamm ◽  
Jennifer M. Streit ◽  
David J. Farrell ◽  
Ronald N. Jones
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Bacterial Pathogens ◽  
Surveillance Program ◽  
Broth Microdilution ◽  
Methicillin Resistant ◽  
Content Type ◽  
Medical Centers ◽  
Resistant Strains

ABSTRACTA total of 84,704 isolates were collected from 191 medical centers in 2009 to 2013 and tested for susceptibility to ceftaroline and comparator agents by broth microdilution methods. Ceftaroline inhibited allStaphylococcus aureusisolates at ≤2 μg/ml and was very active against methicillin-resistant strains (MIC at which 90% of the isolates tested are inhibited [MIC90], 1 μg/ml; 97.6% susceptible). AmongStreptococcus pneumoniaeisolates, the highest ceftaroline MIC was 0.5 μg/ml, and ceftaroline activity against the most commonEnterobacteriaceaespecies (MIC50, 0.12 μg/ml; 78.9% susceptible) was similar to that of ceftriaxone (MIC50, ≤0.25 μg/ml; 86.8% susceptible).

The inositol phosphatase SHIP-1 is negatively regulated by Fli-1 and its loss accelerates leukemogenesis

Blood ◽  
2010 ◽  
Vol 116 (3) ◽  
pp. 428-436 ◽  
Author(s):  
Gurpreet K. Lakhanpal ◽  
Laura M. Vecchiarelli-Federico ◽  
You-Jun Li ◽  
Jiu-Wei Cui ◽  
Monica L. Bailey ◽  
...  
Keyword(s):  
Leukemia Virus ◽  
Signal Transduction Pathway ◽  
Erythroid Differentiation ◽  
Sh2 Domain ◽  
Mitogen Activated Protein Kinase ◽  
Erythroid Progenitors ◽  
Genetic Event ◽  
Ras Pathway ◽  
Inositol Phosphatase ◽  
Mitogen Activated Protein

Abstract The activation of Fli-1, an Ets transcription factor, is the critical genetic event in Friend murine leukemia virus (F-MuLV)–induced erythroleukemia. Fli-1 overexpression leads to erythropoietin-dependent erythroblast proliferation, enhanced survival, and inhibition of terminal differentiation, through activation of the Ras pathway. However, the mechanism by which Fli-1 activates this signal transduction pathway has yet to be identified. Down-regulation of the Src homology 2 (SH2) domain-containing inositol-5-phosphatase-1 (SHIP-1) is associated with erythropoietin-stimulated erythroleukemic cells and correlates with increased proliferation of transformed cells. In this study, we have shown that F-MuLV–infected SHIP-1 knockout mice display accelerated erythroleukemia progression. In addition, RNA interference (RNAi)-mediated suppression of SHIP-1 in erythroleukemia cells activates the phosphatidylinositol 3-kinase (PI 3-K) and extracellular signal-regulated kinase/mitogen-activated protein kinase (ERK/MAPK) pathways, blocks erythroid differentiation, accelerates erythropoietin-induced proliferation, and leads to PI 3-K–dependent Fli-1 up-regulation. Chromatin immunoprecipitation and luciferase assays confirmed that Fli-1 binds directly to an Ets DNA binding site within the SHIP-1 promoter and suppresses SHIP-1 transcription. These data provide evidence to suggest that SHIP-1 is a direct Fli-1 target, SHIP-1 and Fli-1 regulate each other in a negative feedback loop, and the suppression of SHIP-1 by Fli-1 plays an important role in the transformation of erythroid progenitors by F-MuLV.

Bacteremia With Otitis Media

PEDIATRICS ◽  
1991 ◽  
Vol 87 (1) ◽  
pp. 48-53 ◽  
Author(s):  
Sara A. Schutzman ◽  
Stephen Petrycki ◽  
Gary R. Fleisher
Keyword(s):  
Staphylococcus Aureus ◽  
Streptococcus Pneumoniae ◽  
Blood Culture ◽  
Haemophilus Influenzae ◽  
Otitis Media ◽  
Potential Benefit ◽  
Blood Cultures ◽  
Children At Risk ◽  
Focus Of Infection ◽  
Persistent Bacteremia

To investigate the occurrence and outcome of bacteremia associated with otitis media, charts were reviewed from patients who were 3 to 36 months of age, had temperatures ≥39°C, and were diagnosed with isolated clinical otitis media. A total of 2982 patients were identified. Blood cultures were obtained from 1666 (56%). Of the 1666 patients, who had blood drawn for cultures, 50 (3.0%) had bacteremia. These included 39 with Streptococcus pneumoniae, 4 with Haemophilus influenzae, 2 with Neisseria meningitidis, 3 with Salmonella species, and 2 with Staphylococcus aureus. The incidence of bacteremia increased at higher temperatures, being 1.9% at temperatures ≤40°C and 5.0% at temperatures >40°C. Younger children were more likely to have bacteremia; 3.7% ≤12 months of age, 2.4% 13 to 24 months of age, and 1.9% 25 to 36 months of age had blood culture results that were positive (not significant). Reevaluation of the 50 bacteremic patients showed that 9 patients had continued fever, 3 patients had persistent bacteremia, pneumonia developed in 1 patient, and meningitis developed in 1 patient. It was concluded that (1) 3% of young febrile children with otitis media have bacteremia at the time of evaluation, a rate comparable to that previously reported in children with no focus of infection; (2) the incidence of bacteremia increases at higher temperatures; and (3) most febrile children with otitis media do well. The clinician must therefore weigh the potential benefit of drawing a blood culture to identify children at risk for complications against the inherent cost, inconvenience, and discomfort.

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