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  • 1 Laboratory of Functional Genomics, Biological Research Center P.O. Box 521, H-6701 Szeged, Hungary
  • | 2 Department of Pathology University of Szeged, Szeged, Hungary
  • | 3 Department of Pathology University of Szeged, Szeged, Hungary
  • | 4 Department of Pharmacology and Pharmacotherapy University of Szeged, Szeged, Hungary
  • | 5 Department of Pathology University of Szeged, Szeged, Hungary
  • | 6 I: Research Unit for Cardiovascular Pharmacology of the Hungarian Academy of Sciences; II: Department of Pharmacology and Pharmacotherapy; I: P.O. Box 521, H-6701 Szeged, Hungary; II: University of Szeged, Szeged, Hungary;
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Recent and historical evidence is consistent with the view that atherosclerosis is an infectious disease or microbial toxicosis impacted by genetics and behavior. Because small bacterial-like particles, also known as nanobacteria have been detected in kidney stones, kidney and liver cyst fluids, and can form a calcium apatite coat we posited that this agent is present in calcified human atherosclerotic plaques. Carotid and aortic atherosclerotic plaques and blood samples collected at autopsy were examined for nanobacteria-like structures by light microscopy (hematoxylin-eosin and a calcium-specific von Kossa staining), immuno-gold labeling for transmission electron microscopy (TEM) for specific nanobacterial antigens, and propagation from homogenized, filtered specimens in culture medium. Nanobacterial antigens were identified in situ by immuno-TEM in 9 of 14 plaque specimens, but none of the normal carotid or aortic tissue (5 specimens). Nanobacteria-like particles were propagated from 26 of 42 sclerotic aorta and carotid samples and were confirmed by dot immunoblot, light microscopy and TEM. [3H]L-aspartic acid was incorporated into high molecular weight compounds of demineralized particles. PCR amplification of 16S rDNA sequences from the particles was unsuccessful by traditional protocols. Identification of nanobacteria-like particles at the lesion supports, but does not by itself prove the hypothesis that these agents contribute to the pathogenesis of atherosclerosis, especially vascular calcifications.

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Editorial Board

      Csányi, Vilmos (Göd)
      Dudits, Dénes (Szeged)
      Falus, András (Budapest)
      Fischer, Ernő (Pécs)
      Gábriel, Róbert (Pécs)
      Gulya, Károly (Szeged)
      Gulyás, Balázs (Stockholm)
      Hajós, Ferenc (Budapest)
      Hámori, József (Budapest)
      Heszky, László (Gödöllő)
      Hideg, Éva (Szeged)
      E. Ito (Sanuki)
      Janda, Tibor (Martonvásár)
      Kavanaugh, Michael P. (Missoula)
      Kása, Péter (Szeged)
      Klein, Éva (Stockholm)
      Kovács, János (Budapest)
      Brigitte Mauch-Mani (Neuchâtel)
      Nässel, Dick R. (Stockholm)
      Nemcsók, János (Szeged)
      Péczely, Péter (Gödöllő)
      Roberts, D. F. (Newcastle-upon-Tyne)
      Sakharov, Dimitri A. (Moscow)
      Singh, Meharvan (Fort Worth)
      Sipiczky, Mátyás (Debrecen)
      Szeberényi, József (Pécs)
      Székely, György (Debrecen)
      Tari, Irma (Szeged)
      Vágvölgyi, Csaba (Szeged),
      L. Zaborszky (Newark)

 

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Acta Biologica Hungarica
Language English
Size  
Year of
Foundation
1950
Publication
Programme
changed title
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per Year
 
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per Year
 
Founder Magyar Tudományos Akadémia
Founder's
Address
H-1051 Budapest, Hungary, Széchenyi István tér 9.
Publisher Akadémiai Kiadó
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Address
H-1117 Budapest, Hungary 1516 Budapest, PO Box 245.
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Publisher
Chief Executive Officer, Akadémiai Kiadó
ISSN 0236-5383 (Print)
ISSN 1588-256X (Online)