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. 2024 Mar 5;14(5):546.
doi: 10.3390/diagnostics14050546.

Enterobacterales Biofilm-Specific Genes and Antimicrobial and Anti-Inflammatory Biomarkers in the Blood of Patients with Ischemic Heart Disease

Affiliations

Enterobacterales Biofilm-Specific Genes and Antimicrobial and Anti-Inflammatory Biomarkers in the Blood of Patients with Ischemic Heart Disease

Agne Giedraitiene et al. Diagnostics (Basel). .

Abstract

Background: Ischemic heart disease (IHD) is the most prevalent type of cardiovascular disease. The main cause of IHD is atherosclerosis, which is a multifactorial inflammatory disease of blood vessels. Studies show that bacteria might have a significant impact on the pathogenesis of atherosclerosis and plaque rupture. This study aimed to evaluate the complexity of interactions between bacteria and the human body concerning metabolites and bacterial genes in patients with ischemic heart disease.

Methods: Bacterial 16S rDNA and wcaF, papC, and sdhC genes were detected in whole blood using a real-time PCR methodology. An enzyme-linked immunosorbent assay was used to measure the concentration of the LL-37 protein. An analysis of ARA in blood plasma was performed.

Results: Bacterial 16S rDNA was detected in 31% of the study patients, and the genes wcaF and sdhC in 20%. Enterobacterales genes were detected more frequently in patients younger than 65 years than in patients aged 65 years and older (p = 0.018) and in patients with type 2 diabetes (p = 0.048). Concentrations of the human antimicrobial peptide LL-37 and 12S-HETE concentrations were determined to be higher if patients had 16S rDNA and biofilm-specific genes.

Conclusions: The results of this study enhance the understanding that Enterobacterales bacteria may participate in the pathogenesis of atherosclerosis and IHD. Bacterial DNA and host metabolites in higher concentrations appear to be detected.

Keywords: E. coli; bacterial DNA; biofilm; blood direct PCR; cardiovascular diseases; ischemic heart disease.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Flowchart. Study design including exclusion and inclusion criteria and performed procedures.
Figure 2
Figure 2
The scheme shows possible mechanisms of interaction between bacteria and host metabolites arachidonic acid (ARA) and LL-37. (A) ARA and LL-37 attack bacterial membranes; (B) Atherosclerosis in blood vessels, bacteria in biofilms, high ARA metabolites produced by COX, high LL-37 levels.

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