title: Skin own bacteria may aggravate inflammatory and occlusive changes in atherosclerotic arteries of lower limbs.
abstract: OBJECTIVE
  Seroepidemiological studies have given rise to the hypothesis that microorganisms like Chlamydia pneumoniae (CP), Helicobacter pylori (HP), cytomegalovirus (CMV), HCV types 1 and 2, and bacteria involved in dental or other unspecified infection sites may initiate or maintain the atherosclerotic process in lower limb arteries. However, not much attention has been attached to the patient's own limb skin and deep tissues bacterial flora, activated in ischemic tissues. This flora may enhance the inflammatory and thrombotic process in the atherosclerotic arteries. Lower limb tissues are exposed to microorganisms from the environment (foot) and microbes on floating epidermal cells from the perineal and anal regions. The aim of this paper was to identify microbial cells and their DNA in perivascular tissues and arterial walls of lower limbs.
  
  
  METHODS
  Bacterial cultures and PCR method for detection of 16sRNA and immunohistopathological staining for identification of immune cells infiltrating vascular bundles.
  
  
  RESULTS
  1) specimens of atherosclerotic calf and femoral arteries contained bacterial isolates and/or their DNA, whereas, in control normal cadaveric organ donors' limb arteries or patients' carotid arteries and aorta bacteria they were detected only sporadically; 2) lower limb lymphatics contained bacterial cells in 76% of specimens, whereas controls only in 10%; 3) isolates from limb arteries and lymphatics belonged in majority to the coagulase-negative staphylococci and S.aureus, however, other highly pathogenic strains were also detected; 4) immunohistopathological evaluation arterial walls showed dense focal infiltrates of granulocytes and macrophages.
  
  
  CONCLUSIONS
  Own bacterial isolates can be responsible for dense neutrophil and macrophage inflitrates of atherosclerotic walls and periarterial tissue in lower limbs and aggravate the ischemic changes.
authors.affiliation: Department of Surgical Research and Transplantology, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
authors.forename: P
authors.initials: P
authors.lastname: Andziak
authors.forename: W L
authors.initials: WL
authors.lastname: Olszewski
authors.forename: M
authors.initials: M
authors.lastname: Moscicka-Wesolowska
authors.forename: B
authors.initials: B
authors.lastname: Interewicz
authors.forename: E
authors.initials: E
authors.lastname: Swoboda
authors.forename: E
authors.initials: E
authors.lastname: Wastelmach
mesh_terms: D000368:Aged; D050197:Atherosclerosis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D016022:Case-Control Studies; D005260:Female; D005263:Femoral Artery / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D006098:Granulocytes / Q000276:immunology / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D035002:Lower Extremity / Q000098:blood supply*; D042601:Lymphatic Vessels / Q000382:microbiology; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011150:Popliteal Artery / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery; D021521:Ribotyping; D012867:Skin / Q000382:microbiology*; D013210:Staphylococcus / Q000145:classification / Q000235:genetics / Q000302:isolation & purification*; D013211:Staphylococcus aureus / Q000302:isolation & purification; D016909:Tibial Arteries / Q000276:immunology / Q000382:microbiology* / Q000473:pathology / Q000601:surgery