Periodontal Bacterial DNA and Their Link to Human Cardiac Tissue: Findings of a Pilot Study

2015 ◽  
Vol 66 (01) ◽  
pp. 083-090 ◽  
Author(s):  
Dirk Ziebolz ◽  
Christoph Rost ◽  
Julia Schmidt ◽  
Regina Waldmann-Beushausen ◽  
Friedrich Schöndube ◽  
...  
Keyword(s):  
Pilot Study ◽  
Aortic Valve ◽  
Cardiac Tissue ◽  
Binding Protein ◽  
Myocardial Revascularization ◽  
Tissue Samples ◽  
Bacterial Dna ◽  
Protocol Biopsies ◽  
Human Cardiac Tissue ◽  
Lps Binding

Background The aim of this pilot study was to detect correlations of microbiological DNA, inflammatory proteins, and infection parameters in patients with periodontal disease (PD) and valvular heart disease (VHD). Methods A perioperative comprehensive dental examination for the investigation of periodontal status, including sampling of specific subgingival bacteria, was performed in 10 patients with indication for surgery of aortic valve stenosis with or without concomitant myocardial revascularization. Standard protocol biopsies were taken from right atrium (A), left septal myocardium (M), and aortic valve (V). Eleven periodontal pathogens DNA in oral and cardiac tissue samples (A/M/V) were analyzed using polymerase chain reaction. For cardiac tissue samples, Western blot analysis of LPS-binding protein (LBP), immunohistochemical (IHC) detection of LBP-big42, LPS-binding protein receptor (CD14), and macrophages (CD68), as well as inflammation scoring measurement were performed. Results Periodontitis was present in all patients with severe intensity in 7, moderate in 2 and mild in one patient. Same bacterial DNA was detected in A, M, and V in different distribution, and detection was more often in atrium than in myocardium or valve tissue. Morphological investigation revealed increased extracellular inflammatory cell migration. In IHC markers of LBP, CD68 and CD14 showed positive findings for all patients in atrium and myocardium. Conclusion Our results demonstrate the presence of oral bacterial DNA in human cardiac tissue, as well as inflammatory markers potentially indicating connection of PD and VHD. Further investigation is necessary to confirm these preliminary data.

The Nonselective β-Blocker Carvedilol Suppresses Apoptosis in Human Cardiac Tissue: A Pilot Study

2010 ◽  
Vol 13 (4) ◽  
pp. E218-E222 ◽  
Author(s):  
Engin Usta ◽  
Migdat Mustafi ◽  
Andreas Straub ◽  
Gerhard Ziemer
Keyword(s):  
Pilot Study ◽  
Cardiac Tissue ◽  
Β Blocker ◽  
Human Cardiac Tissue

Correlation of DNA, LPS-binding-protein and CD14 of periodontal microbes and cardiac tissue-preliminary results

2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
B.C. Danner ◽  
D. Ziebolz ◽  
C. Rost ◽  
J. Schmidt ◽  
R. Waldmann-Beushausen ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
Binding Protein ◽  
Preliminary Results ◽  
Lps Binding

scholarly journals Amyloidosis, Inflammation, and Oxidative Stress in the Heart of an Alkaptonuric Patient

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Lia Millucci ◽  
Lorenzo Ghezzi ◽  
Eugenio Paccagnini ◽  
Giovanna Giorgetti ◽  
Cecilia Viti ◽  
...  
Keyword(s):  
Aortic Valve ◽  
Autosomal Recessive ◽  
Cardiac Tissue ◽  
Light And Electron Microscopy ◽  
Secondary Amyloidosis ◽  
Tissue Degeneration ◽  
Amyloid Deposits ◽  
Biochemical Assays ◽  
Human Cardiac Tissue ◽  
And Oxidative Stress

Background. Alkaptonuria, a rare autosomal recessive metabolic disorder caused by deficiency in homogentisate 1,2-dioxygenase activity, leads to accumulation of oxidised homogentisic acid in cartilage and collagenous structures present in all organs and tissues, especially joints and heart, causing a pigmentation called ochronosis. A secondary amyloidosis is associated with AKU. Here we report a study of an aortic valve from an AKU patient.Results. Congo Red birefringence, Th-T fluorescence, and biochemical assays demonstrated the presence of SAA-amyloid deposits in AKU stenotic aortic valve. Light and electron microscopy assessed the colocalization of ochronotic pigment and SAA-amyloid, the presence of calcified areas in the valve. Immunofluorescence detected lipid peroxidation of the tissue and lymphocyte/macrophage infiltration causing inflammation. High SAA plasma levels and proinflammatory cytokines levels comparable to those from rheumatoid arthritis patients were found in AKU patient.Conclusions. SAA-amyloidosis was present in the aortic valve from an AKU patient and colocalized with ochronotic pigment as well as with tissue calcification, lipid oxidation, macrophages infiltration, cell death, and tissue degeneration. A localHGDexpression in human cardiac tissue has also been ascertained suggesting a consequent local production of ochronotic pigment in AKU heart.

scholarly journals Interindividual heterogeneity affects the outcome of human cardiac tissue decellularization

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Miguel F. Tenreiro ◽  
Henrique V. Almeida ◽  
Tomás Calmeiro ◽  
Elvira Fortunato ◽  
Lino Ferreira ◽  
...  
Keyword(s):  
Cardiac Tissue ◽  
Sodium Dodecyl ◽  
Cell Alignment ◽  
Tissue Samples ◽  
Cardiac Tissues ◽  
Human Cardiac Tissue ◽  
Induced Pluripotent ◽  
Ecm Architecture ◽  
Triton X ◽  
Extended Exposure

AbstractThe extracellular matrix (ECM) of engineered human cardiac tissues corresponds to simplistic biomaterials that allow tissue assembly, or animal derived off-the-shelf non-cardiac specific matrices. Decellularized ECM from human cardiac tissue could provide a means to improve the mimicry of engineered human cardiac tissues. Decellularization of cardiac tissue samples using immersion-based methods can produce acceptable cardiac ECM scaffolds; however, these protocols are mostly described for animal tissue preparations. We have tested four methods to decellularize human cardiac tissue and evaluated their efficiency in terms of cell removal and preservation of key ECM components, such as collagens and sulfated glycosaminoglycans. Extended exposure to decellularization agents, namely sodium dodecyl sulfate and Triton-X-100, was needed to significantly remove DNA content by approximately 93% in all human donors. However, the biochemical composition of decellularized tissue is affected, and the preservation of ECM architecture is donor dependent. Our results indicate that standardization of decellularization protocols for human tissue is likely unfeasible, and a compromise between cell removal and ECM preservation must be established in accordance with the scaffold’s intended application. Notwithstanding, decellularized human cardiac ECM supported human induced pluripotent-derived cardiomyocyte (hiPSC-CM) attachment and retention for up to 2 weeks of culture, and promoted cell alignment and contraction, providing evidence it could be a valuable tool for cardiac tissue engineering.

Kupffer cell activation by LPS is mediated via LPS binding protein and CD14

2001 ◽  
Vol 120 (5) ◽  
pp. A27-A27
Author(s):  
M FAN ◽  
S GOYERT ◽  
A AMINLARI ◽  
R KLEIN ◽  
L STEINSTRAESSER ◽  
...  
Keyword(s):  
Kupffer Cell ◽  
Cell Activation ◽  
Binding Protein ◽  
Lps Binding

Hemoglobin Enhances the Binding of Bacterial Endotoxin to Human Endothelial Cells

1996 ◽  
Vol 76 (02) ◽  
pp. 258-262 ◽  
Author(s):  
Robert I Roth
Keyword(s):  
Endothelial Cells ◽  
Binding Protein ◽  
Bacterial Endotoxin ◽  
Dependent Manner ◽  
Serum Free Medium ◽  
Free Medium ◽  
Human Endothelial Cells ◽  
Serum Factors ◽  
Serum Free ◽  
Lps Binding

SummaryHuman endothelial cells, when incubated with bacterial endotoxin (lipopolysaccharide, LPS), modify their surface in association with prominent production of procoagulant tissue factor (TF) activity. This deleterious biological effect of LPS has been shown previously to be enhanced approximately 10-fold by the presence of hemoglobin (Hb), a recently recognized LPS binding protein that causes disaggregation of LPS and increases the biological activity of LPS in a number of in vitro assays. The present study was performed to test the hypothesis that Hb enhances the LPS-induced procoagulant activity of human umbilical vein endothelial cells (HUVEC) by increasing LPS binding to the cells. The binding of 3H-LPS to HUVEC was determined in the absence or presence of Hb or two other known LPS-binding proteins, human serum albumin (HSA) and IgG. LPS binding was substantially increased in the presence of Hb, in a Hb concentration-dependent manner, but was not increased by HSA or IgG. Hb enhancement of LPS binding was observed in serum-free medium, indicating that there was no additional requirement for any of the serum factors known to participate in the interaction of LPS with cells (e.g., lipopolysaccharide (LPS)-binding protein (LBP) and soluble CD14 (sCD14)). Hb enhancement of LPS binding also was observed in the more physiologic condition of 100% plasma. LPS-induced TF activity was stimulated by Hb, but not by HSA or IgG. In serum-free medium, TF activity was not stimulated under any of the conditions tested. Ultrafiltration of LPS was dramatically increased after incubation with Hb but not with HSA or IgG, suggesting that LPS disaggregation by Hb was responsible for the enhanced binding of LPS to HUVEC and the subsequent stimulation of TF activity.

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