scholarly journals Streptococcus gordonii DL1 evades polymorphonuclear leukocyte-mediated killing via resistance to lysozyme

PLoS ONE ◽  
2021 ◽  
Vol 16 (12) ◽  
pp. e0261568
Author(s):  
Yumiko Urano-Tashiro ◽  
Keitarou Saiki ◽  
Yuki Yamanaka ◽  
Yuiko Ishikawa ◽  
Yukihiro Takahashi
Keyword(s):  
Hydrogen Peroxide ◽  
Infective Endocarditis ◽  
High Resistance ◽  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Low Ph ◽  
Streptococcus Gordonii ◽  
Bactericidal Assay ◽  
Bacterial Agent

Streptococcus gordonii is an etiological bacterial agent of infective endocarditis. Although the pathogenesis mechanisms are not well understood, the interaction between streptococci and phagocytes is considered important for the development of infective endocarditis. Previous studies show that some S. gordonii strains, including DL1, survive in polymorphonuclear leukocytes (PMNs), whereas other strains such as SK12 are sensitive to PMN-dependent killing. In this study, we assessed the differences between the sensitivity of S. gordonii DL1 and S. gordonii SK12 to PMN-dependent killing. S. gordonii DL1 showed a higher survival when treated with PMNs than SK12. Both S. gordonii DL1 and S. gordonii SK12 showed high resistance to low pH condition. Compared to S. gordonii SK12, S. gordonii DL1 was sensitive to hydrogen peroxide. However, the resistance of S. gordonii DL1 to the tested bactericidal agents, especially lysozyme, was higher than that of SK12. Furthermore, we performed a bactericidal assay by treating a mixture of S. gordonii DL1 and SK12 with PMNs. S. gordonii DL1 did not enhance the survival of S. gordonii SK12 exposed to PMNs. These results indicated that S. gordonii DL1 is resistant to bactericidal agents that degrade bacteria in phagolysosomes. In addition, there was no secretory factor involved in the resistance to bactericidal agents. The findings of this study may help develop treatments for infective endocarditis caused by S. gordonii.

scholarly journals Resistance of Streptococcus gordonii to Polymorphonuclear Leukocyte Killing Is a Potential Virulence Determinant of Infective Endocarditis

2006 ◽  
Vol 74 (6) ◽  
pp. 3148-3155 ◽  
Author(s):  
Si Young Lee ◽  
John O. Cisar ◽  
Joseph L. Bryant ◽  
Michael A. Eckhaus ◽  
Ann L. Sandberg
Keyword(s):  
Infective Endocarditis ◽  
Polymorphonuclear Leukocytes ◽  
Severe Disease ◽  
Human Platelets ◽  
Avirulent Strain ◽  
Streptococcus Gordonii ◽  
Aortic Valves ◽  
Superoxide Anion Production ◽  
Virulence Determinant ◽  
Virulent Strains

ABSTRACT Significant differences in virulence among seven representative Streptococcus gordonii strains were observed by using the rat model of infective endocarditis. Five strains, including S. gordonii DL1, caused severe disease, while the other two strains, including S. gordonii SK12, caused minimal or no disease. The differences in virulence were evident from the visible presence of streptococci in the vegetations present on the aortic valves of catheterized rats that were challenged with individual strains and also from the much greater recovery of rifampin-resistant S. gordonii DLl than of streptomycin-resistant S. gordonii SK12 from the hearts of animals coinfected with both organisms. Each S. gordonii strain aggregated with human platelets and bound to polymorphonuclear leukocytes (PMNs), as shown by the stimulation of PMN superoxide anion production. These interactions were reduced or abolished by pretreatment of the platelets or PMNs with sialidase, indicating that there was bacterial recognition of host sialic acid-containing receptors. Adhesin-mediated binding of each S. gordonii strain to PMNs also triggered phagocytosis. However, the subsequent PMN-dependent killing differed significantly for the seven strains. The five virulent strains included three strains that were not killed and two strains whose numbers were reduced by approximately 50%. In contrast, the level of killing of each avirulent strain under the same conditions was significantly greater and approached 90% of the bacteria added. Parallel studies performed with rat PMNs revealed comparable differences in the resistance or susceptibility of representative virulent and avirulent strains. Thus, the ability of S. gordonii to survive in PMNs following adhesin-mediated phagocytosis may be an important virulence determinant of infective endocarditis.

scholarly journals Intracranial bleeding (ICB) as a catastrophic complication of Streptococcus gordonii infective endocarditis (IE) in an immunocompetent patient

2018 ◽  
pp. bcr-2018-225265
Author(s):  
Mohd Shakirin Pairan ◽  
Nurashikin Mohammad ◽  
Sanihah Abdul Halim ◽  
Wan Syamimee Wan Ghazali
Keyword(s):  
Infective Endocarditis ◽  
Late Onset ◽  
Mass Effect ◽  
Immunocompetent Patient ◽  
Interesting Case ◽  
Vascular Complication ◽  
Intracranial Bleeding ◽  
Streptococcus Gordonii ◽  
Ct Angiogram ◽  
Ct Brain

We present an interesting case of late-onset intracranial bleeding (ICB) as a complication of Streptococcus gordonii causing infective endocarditis. A previously healthy young woman was diagnosed with infective endocarditis. While she was already on treatment for 2 weeks, she had developed seizures with a localising neurological sign. An urgent non-contrasted CT brain showed massive left frontoparietal intraparenchymal bleeding. Although CT angiogram showed no evidence of active bleeding or contrast blush, massive ICB secondary to vascular complication of infective endocarditis was very likely. An urgent decompressive craniectomy with clot evacuation was done immediately to release the mass effect. She completed total 6 weeks of antibiotics and had postoperative uneventful hospital stay despite having a permanent global aphasia as a sequel of the ICB.

scholarly journals Intracellular localization of Rickettsia tsutsugamushi in polymorphonuclear leukocytes.

1979 ◽  
Vol 150 (3) ◽  
pp. 703-708 ◽  
Author(s):  
Y Rikihisa ◽  
S Ito
Keyword(s):  
Guinea Pig ◽  
Cell Cultures ◽  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Intracellular Localization ◽  
The Other ◽  
Cytoplasmic Organelles

Rickettsia tsutsugamushi (Gilliam strain) was serially propagated in BHK-21 cell cultures and incubated with guinea pig peritoneal polymorphonuclear leukocytes to study the ultrastructural features of rickettsial uptake and entry into the leukocytes. Significant numbers of rickettsiae were phagocytized selectively by these leukocytes within 30 min. About one-half of these rickettsiae remained sequestered in phagosomes but the other one-half were free from the phagosome and localized directly in the polymorphonuclear leukocyte cytoplasm. Various stages of rickettsial release from the phagosomes were observed. Once free within the polymorphonuclear leukocyte cytoplasm, the rickettsiae were preferentially localized in the glycogen-packed areas which are devoid of lysosomes and other cytoplasmic organelles. This study indicates that rickettsiae phagocytized by polymorphonuclear leukocytes can escape from the phagosome into the cytoplasm.

scholarly journals Effect of Nedocromil Sodium on Polymorphonuclear Leukocyte Plasma Membrane

1994 ◽  
Vol 3 (7) ◽  
pp. S21-S24 ◽  
Author(s):  
A. Kantar ◽  
N. Oggiano ◽  
P. L. Giorgi ◽  
G. V. Coppa ◽  
R. Gabbianelli ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Steady State ◽  
Membrane Fluidity ◽  
Fluorescence Anisotropy ◽  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Plasma Membranes ◽  
Nedocromil Sodium ◽  
Plasma Membrane Fluidity ◽  
Steady State Fluorescence

The effect of nedocromil sodium on the plasma membrane fluidity of polymorphonuclear leukocytes (PMNs) was investigated by measuring steady-state fluorescence anisotropy of 1-[4-trimethylammonium-phenyl]-6-phenyl- 1,3,5-hexatriene (TMA-DPH) incorporated in the membrane. Our results show that nedocromil sodium 300 μM significantly decreased membrane fluidity of PMNs. The decrease in membrane fluidity of PMNs induced by fMLP was abolished in the presence of nedocromil sodium. These data suggest that nedocromil sodium interferes with the plasma membranes of PMNs and modulates their activities.

Effect of Some Anti-Inflammatory Drugs on Human Neutrophil Chemotaxis

1994 ◽  
Vol 22 (2) ◽  
pp. 100-106 ◽  
Author(s):  
G Hasçelik ◽  
B ŞLener ◽  
Z Hasçelik
Keyword(s):  
Acetylsalicylic Acid ◽  
Polymorphonuclear Leukocyte ◽  
Polymorphonuclear Leukocytes ◽  
Diclofenac Sodium ◽  
Tiaprofenic Acid ◽  
Boyden Chamber ◽  
Random Migration ◽  
Leukocyte Chemotaxis ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

The effects of piroxicam, tenoxicam, diclofenac sodium, acetylsalicylic acid and tiaprofenic acid on the chemotaxis and random migration of human polymorphonuclear leukocytes were investigated, using zymosan-activated serum as chemo-attractant, with a modified Boyden chamber technique. All five compounds significantly reduced chemotaxis. The random migration of polymorphonuclear leukocytes was inhibited by piroxicam, diclofenac sodium and tiaprofenic acid but not by tenoxicam or acetylsalicylic acid. The inhibitory effect of these non-steroidal anti-inflammatory drugs on polymorphonuclear leukocyte chemotaxis and on random migration was generally dose-dependent. The results suggest that the drugs studied may have a direct effect on polymorphonuclear leukocyte chemotaxis and that this activity may contribute to their anti-inflammatory properties.

BACTERICIDAL FUNCTION OF HUMAN POLYMORPHONUCLEAR LEUKOCYTES

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 264-270
Author(s):  
Paul G. Quie
Keyword(s):  
Hydrogen Peroxide ◽  
Chronic Granulomatous Disease ◽  
Polymorphonuclear Leukocytes ◽  
Bacterial Species ◽  
Bacterial Flora ◽  
Granulomatous Disease ◽  
Serum Factors ◽  
Gram Negative ◽  
Increased Risk ◽  
Human Polymorphonuclear Leukocytes

Serum from most normal persons contains specific antibodies which react with common bacterial species preparing their surfaces so that phagocytosis by leukocytes can take place. The Fab part of these antibodies reacts with immunologic specificity with antigens on the surface of bacteria. Another part of the immunoglobulin molecule termed the Fc portion is activated during the attachment of the Fab portion to bacteria and becomes a site for attachment of bacteria to receptors on the surface of phagocytic cells. This activity is greatly amplified by heat-labile serum factors. Normally bacteria are rapidly killed by human polymorphonuclear leukocytes after engulfment occurs. However staphylococci and gram-negative species of bacteria survive in the leukocytes of patients with the syndrome "Chronic Granulomatous Disease of Childhood." These patients have suffered recurrent severe infections with bacterial species that are part of the body's resident bacterial flora. By contrast these patients are not at increased risk to infection from such pyogenic bacterial species as group A streptococci or pneumococci. The leukocytes from patients with chronic granulomatous disease produce little hydrogen peroxide during phagocytosis. Catalase-producing staphylococci and gram-negative bacteria are not killed, but hydrogen peroxide-producing streptococci and pneumococci are killed. A normal metabolic response to phagocytosis as well as release of lysosonial factors are essential for the bactericidal activity of human polymorphonuclear leukocytes.

Source of hydrogen peroxide and of chemiluminescence observed in activated human platelet preparations

Blood ◽  
1977 ◽  
Vol 50 (4) ◽  
pp. 597-602 ◽  
Author(s):  
NI Krinsky ◽  
KL Scoon ◽  
JC Hardin ◽  
PH Levine
Keyword(s):  
Hydrogen Peroxide ◽  
Polymorphonuclear Leukocytes ◽  
Human Platelet ◽  
H2o2 Production ◽  
Activated Platelets ◽  
Latex Spheres

Abstract Human platelet suspensions can be observed to produce small amounts of H2O2 (0.04 nmoles H2O2/min/2.5 X 10(5) cells/cu mm) and measurable chemiluminescence when exposed to target particles for phagocytosis, such as latex spherules. Both H2O2 production and chemiluminescence are characteristic of phagocytosing polymorphonuclear leukocytes (PMN) and analysis of the purified platelets indicates contamination by PMN at the level of 0.2%. The amount of H2O2 produced and the chemiluminescence observed can be duplicated by adding latex spheres to a preparation of PMN at a concentration equivalent to the contaminant in the platelet preparations. We conclude that the H2O2 produced and chemiluminescence observed from activated platelets is due to the presence of small amounts of contaminating PMN. These studies emphasize the importance of controlling for PMN contamination in studies of platelet biochemistry and physiology.

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