Streptococcus salivarius Promotes Mucin Putrefaction and Malodor Production by Porphyromonas gingivalis

2006 ◽  
Vol 85 (10) ◽  
pp. 910-914 ◽  
Author(s):  
N. Sterer ◽  
M. Rosenberg

Although the contribution of the oral microbiota to oral malodor is well-documented, the potential role of Gram-positive micro-organisms is unclear. In the current study, we tested the hypothesis that Gram-positive micro-organisms contribute to malodor production by deglycosylating oral glycoproteins, rendering them susceptible to subsequent proteolysis. To this end, we examined the effect of Streptococcus salivarius on Porphyromonas gingivalis-mediated putrefaction of a model glycoprotein (pig gastric mucin). Malodor was scored by two odor judges, and volatile sulfides were determined with the use of a sulfide monitor. Mucin degradation was followed by electrophoresis on SDS-PAGE. Results showed that the addition of S. salivarius or β-galactosidase promoted mucin degradation and concomitant malodor production. Addition of glycosidic inhibitors (p-APTG and glucose) inhibited this process. These results suggest that Gram-positive micro-organisms such as S. salivarius contribute to oral malodor production by deglycosylating salivary glycoproteins, thus exposing their protein core to further degradation by Gram-negative micro-organisms.

2013 ◽  
Vol 38 (2) ◽  
pp. 89-96 ◽  
Author(s):  
Ryan P. Moenster ◽  
Travis W. Linneman ◽  
William B. Call ◽  
Chad L. Kay ◽  
Theresa A. McEvoy ◽  
...  
Keyword(s):  

1986 ◽  
Vol 18 (Supplement_E) ◽  
pp. 47-59 ◽  
Author(s):  
F. Baquero ◽  
E. Culebras ◽  
C. Patrón ◽  
J. C. Pérez-Díaz ◽  
J. C. Medrano ◽  
...  

2020 ◽  
Vol 15 (3) ◽  
pp. 031007
Author(s):  
Todd E. Alexander ◽  
Ian M. Smith ◽  
Zachary W. Lipsky ◽  
Lindsay D. Lozeau ◽  
Terri A. Camesano

Author(s):  
Sumalatha D ◽  
Nithya Tg ◽  
Jayanthi J ◽  
Ragunathan Mg

 Objective: The study was done to isolate the antimicrobial protein from the freshwater crab.Methods: Antimicrobial protein was purified by sequential step of ammonium sulfate precipitation, dialysis, ion exchange chromatography, and fast protein liquid chromatography. The apparent molecular mass was determined by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and matrix-assisted laser desorption ionization-mass spectrometry (MALDI-MS/MS). Primary structure analysis was done from MASCOT search engine. The antimicrobial activity of the protein was done using well diffusion method against Gram-positive and Gram-negative bacteria.Results: The molecular mass of antimicrobial protein was determined to be 33KDa by SDS-PAGE and MALDI-MS/MS. The antimicrobial protein contains eight peptides which were determined by MASCOT search engine. The protein exhibited antimicrobial activity both for Gram-positive and Gram-negative bacteria.Conclusion: The results could provide information for investigating the antimicrobial protein derived from the hemolymph of the freshwater crab Oziotelphusa senex senex.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Sonya Urnowey ◽  
Toshihiro Ansai ◽  
Vira Bitko ◽  
Koji Nakayama ◽  
Tadamichi Takehara ◽  
...  

The Editor has retracted this article [1] following an investigation by the University of South Alabama which found:


2020 ◽  
Vol 11 ◽  
Author(s):  
Chiaki Yamada ◽  
Juliet Akkaoui ◽  
Anny Ho ◽  
Carolina Duarte ◽  
Richard Deth ◽  
...  

BackgroundAmong different types of sphingolipids produced by human cells, the possible engagement of ceramide species in the pathogenesis of Alzheimer’s disease (AD) has attracted recent attention. While ceramides are primarily generated by de novo synthesis in mammalian cells, only a limited number of bacterial species, produce ceramides, including phosphoglycerol dihydroceramide (PGDHC) that is produced by the key periodontal pathogen Porphyromonas gingivalis. Emerging evidence indicates that virulence factors produced by P. gingivalis, such as lipopolysaccharide and gingipain, may be engaged in the initiation and/or progression of AD. However, the potential role of PGDHC in the pathogenesis of AD remains unknown. Therefore, the aim of this study was to evaluate the influence of PGDHC on hallmark findings in AD.Material and MethodsCHO-7WD10 and SH-SY-5Y cells were exposed to PGDHC and lipopolysaccharide (LPS) isolated from P. gingivalis. Soluble Aβ42 peptide, amyloid precursor protein (APP), phosphorylated tau and senescence-associated secretory phenotype (SASP) factors were quantified using ELISA and Western blot assays. ResultsOur results indicate that P. gingivalis (Pg)-derived PGDHC, but not Pg-LPS, upregulated secretion of soluble Aβ42 peptide and expression of APP in CHO-7WD10 cells. Furthermore, hyperphosphorylation of tau protein was observed in SH-SY-5Y cells in response to PGDHC lipid. In contrast, Pg-LPS had little, or no significant effect on the tau phosphorylation induced in SH-SY-5Y cells. However, both PGDHC and Pg-LPS contributed to the senescence of SH-SY5Y cells as indicated by the production of senescence-associated secretory phenotype (SASP) markers, including beta-galactosidase, cathepsin B (CtsB), and pro-inflammatory cytokines TNF-α, and IL-6. Additionally, PGDHC diminished expression of the senescence-protection marker sirtuin-1 in SH-SY-5Y cells.ConclusionsAltogether, our results indicate that P. gingivalis-derived PGDHC ceramide promotes amyloidogenesis and hyperphosphorylation, as well as the production of SASP factors. Thus, PGDHC may represent a novel class of bacterial-derived virulence factors for AD associated with periodontitis.


2004 ◽  
Vol 186 (23) ◽  
pp. 7905-7913 ◽  
Author(s):  
Jacobo Zuñiga-Castillo ◽  
David Romero ◽  
Jaime M. Martínez-Salazar

ABSTRACT Single-strand gaps (SSGs) and double-strand breaks (DSBs) are the major initiation sites for recombination. In bacteria, the SSGs are repaired by RecFOR, while the DSBs are processed by RecBCD in gram-negative bacteria and AddAB in gram-positive bacteria. Unexpectedly, instead of recBCD genes, the addAB genes were found in members of the α-proteobacteria group (gram negative). Taking Rhizobium etli as a model, the role of recF and addAB genes in homologous recombination and repair of damaged DNA was evaluated. Inactivation of either recF or addA provoked strong sensitivity to UV radiation and mitomycin C, while an additive effect was observed in the recF-addA mutant. The DSBs generated by nalidixic acid caused low viability only in the addA mutant. The recombination frequency of large and small plasmids was reduced in the recF mutant (24- and 36-fold, respectively), whereas a slight decrease (threefold) in the addA mutant was observed. Moreover, an additive effect (47- and 90-fold, respectively) was observed in the double mutant, but it was not as dramatic as that in a recA mutant. Interestingly, the frequency of deletion and Campbell-type recombination was slightly affected in either single or double mutants. These results suggest that another pathway exists that allows plasmid and Campbell-type recombination in the absence of recF and addA genes.


Shock ◽  
2013 ◽  
Vol 40 (4) ◽  
pp. 290-296 ◽  
Author(s):  
Dana C. Blok ◽  
Alex F. de Vos ◽  
Sandrine Florquin ◽  
Tom van der Poll

1988 ◽  
Vol 2 (2) ◽  
pp. 346-353 ◽  
Author(s):  
C. Chen ◽  
M.E. Wilson

Eikenella corrodens is a facultatively anaerobic Gram-negative bacterium which is among the predominant cultivable microflora of periodontal lesions characterized by loss of attachment level. In the present study, we examined the potential role of complement-mediated killing in host defense against this periodontopathic organism. Seven clinical isolates obtained from human subgingival plaque and one reference strain of E. corrodens were characterized with respect to (a) susceptibility to the bactericidal properties of pooled human serum and (b) the role of the classical and/or alternative pathway(s) of complement in effecting killing of sensitive strains. Six strains, including the reference strain, were found to be variably serum-sensitive, exhibiting 1-12.5% survival after two hr of incubation in the presence of 20% pooled human serum. The remaining two isolates were serum-resistant. Both serum-resistant and serum-sensitive strains consumed complement via the classical pathway in normal but not in hypogammaglobulinemic serum, thus ruling out an antibody-independent mechanism of classical pathway activation. Four of six serum-sensitive strains exhibited little or no loss of viability following incubation with serum depleted of the classical pathway component Clq. One strain which was resistant to killing by normal human serum was, nevertheless, highly susceptible to complement-mediated killing in the presence of rabbit immune serum. Two additional serum-sensitive strains were killed, albeit to a lesser extent, in Clq-depleted serum, indicative of a role of the alternative pathway in killing of some serum-sensitive strains. These results indicate a potential role for complement-mediated killing in host defense against Gram-negative periodontal bacteria such as E. corrodens. However, the ultimate contribution of this immune defense mechanism may be defined, at least in part, by the presence of a humoral response to key bacterial membrane constituents.


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