Abstract
There are an increasing number of data showing a clinically important association
between bacterial infection and peripheral artery disease (PAD). Bacteria suspected
of being involved in PAD pathogenesis are: periodontal bacteria, gut microbiota, Helicobacter pylori, and Chlamydia pneumoniae. Infectious agents may be involved in the pathogenesis of atherosclerosis via activation
of a systemic or local host immunological response to contamination of extravascular
tissues or the vascular wall, respectively. A systemic immunological reaction may
damage vascular walls in the course of autoimmunological cross-reactions between anti-pathogen
antibodies and host vascular antigens (immunological mimicry), pathogen burden mechanisms
(nonspecific activation of inflammatory processes in the vascular wall), and neuroendocrine-immune
cross-talk. Besides activating the inflammatory pathway, bacterial infection may trigger
PAD progression or exacerbation by enhancement of platelet reactivity, by a stimulatory
effect on von Willebrand factor binding, factor VIII, fibrinogen, P-selectin activation,
disturbances in plasma lipids, increase in oxidative stress, and resistance to insulin.
Local inflammatory host reaction and induction of atherosclerotic plaque progression
and/or instability result mainly from atherosclerotic plaque colonization by microorganisms.
Despite these premises, the role of bacterial infection in PAD pathogenesis should
still be recognized as controversial, and randomized, controlled trials are required
to evaluate the outcome of periodontal or gut bacteria modification (through diet,
prebiotics, and probiotics) or eradication (using antibiotics) in hard and surrogate
cardiovascular endpoints.
Keywords
atherosclerosis - peripheral artery disease - bacteria - infection -
Helicobacter pylori
- periodontitis
