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Microbial Modulation of Coagulation Disorders in Venous Thromboembolism

Authors Lichota A, Gwozdzinski K, Szewczyk EM

Received 18 April 2020

Accepted for publication 19 June 2020

Published 30 July 2020 Volume 2020:13 Pages 387—400

DOI https://doi.org/10.2147/JIR.S258839

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Ning Quan


Anna Lichota,1 Krzysztof Gwozdzinski,2 Eligia M Szewczyk1

1Department of Pharmaceutical Microbiology and Microbiological Diagnostics, Faculty of Pharmacy, Medical University of Lodz, Lodz, Poland; 2Department of Molecular Biophysics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland

Correspondence: Anna Lichota Department of Pharmaceutical Microbiology and Microbiological Diagnostics, Faculty of Pharmacy
Medical University of Lodz, Pomorska 137, Lodz 90-235, Poland
Tel +48 426779300
Email anna.lichota@umed.lodz.pl

Abstract: Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), is the third leading cause of cardiovascular death in the world. Important risk factors of thrombosis include bed restraint, surgery, major trauma, long journeys, inflammation, pregnancy, and oral contraceptives, previous venous thromboembolism, cancer, and bacterial infections. Sepsis increases the risk of blood clot formation 2– 20 times. In this review, we discussed various mechanisms related to the role of bacteria in venous thrombosis also taking into consideration the role of the human microbiome. Many known bacteria, such as Helicobacter pylori, Chlamydia pneumoniae, Mycoplasma pneumoniae, Haemophilus influenzae, Streptococcus pneumoniae, Staphylococcus aureus, and Escherichia coli, causing infections may increase the risk of thrombotic complications through platelet activation or may lead to an inflammatory reaction involving the fibrinolytic system. Additionally, the bacteria participate in the production of factors causing or increasing the risk of cardiovascular diseases. An example can be trimethylamine N-oxide (TMAO) but also uremic toxins (indoxyl sulfate), short-chain fatty acids (SCFA) phytoestrogens, and bile acids. Finally, we presented the involvement of many bacteria in the development of venous thromboembolism and other cardiovascular diseases.

Keywords: sepsis, microbiome, inflammation, deep vein thrombosis, trimethylamine N-oxide

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