# Genetic potential for biofilm formation of clinical strains of Pseudomonas aeruginosa

**Authors:** U.М. Nemchenko, N.L. Belkova, E.S. Klimenko, N.E. Smurova, R.E. Zugeeva, V.V. Sinkov, E.D. Savilov

PMC · DOI: 10.18699/vjgb-25-62 · 2025-07-01

## TL;DR

This study explores how clinical strains of Pseudomonas aeruginosa form biofilms, which help them survive in patients with cystic fibrosis.

## Contribution

The study identifies genetic markers linked to biofilm formation in P. aeruginosa strains from cystic fibrosis patients.

## Key findings

- Clinical strains of P. aeruginosa showed moderate biofilm-forming ability with varying coefficients.
- Differences in genes related to biofilm regulation were observed across strains.
- Specific genes like pppA, icmF, and clpV1 showed structural differences useful for strain identification.

## Abstract

Pseudomonas aeruginosa is one of the leading causes of nosocomial respiratory tract infections and plays an important role in lower respiratory tract infection in patients with cystic fibrosis (CF). Biofilms, which are organized cell clusters, ensure the survival of microorganisms in unfavorable environmental conditions and contribute to the chronicity of infection and the formation of persistent forms. The aim of this study was to determine the phenotypic ability and genetic potential for biofilm formation in clinical strains of P. aeruginosa persisting in patients with CF against the background of constant intake of antimicrobial drugs. Bacteriological, genetic, and bioinformatic methods were used to characterize five P. aeruginosa strains obtained from patients with CF. Phenotypically, all strains were classified as moderately biofilm-forming, while the biofilm formation coefficient varied from 2.10 to 3.15. Analysis of draft genomes revealed differences in the representation of some genes or individual loci of three of the four known signaling pathways (cAMP/Vfr, Gac/Rsm, and c-di-GMP) that have been described in P. aeruginosa genomes and are related to the regulation of biofilm formation. In addition, differences in the representation of genes such as frzE, tcpE, and rcsC are shown. Of undoubted interest is the analysis of genes such as pppA, icmF, clpV1, trpE, trpG, and stp1, which are used for extended multilocus typing PubMLST and differed in the structure of loci in all analyzed strains. These genes can be used to identify clinical strains of P. aeruginosa and to characterize their biofilm-forming properties. Thus, genes potentially participating in both biofilm formation and regulation have been characterized in the genomes of clinical P. aeruginosa strains that persist for a long time in patients receiving continuous antibiotic therapy. Characterization of the genetic potential for biofilm formation makes it possible to search for reliable genetic markers of this process in order to monitor the evolution of the pathogen as a result of long-term persistence in the host organism.

## Linked entities

- **Genes:** tcpE (t-complex protein1, epsilon-SU) [NCBI Gene 857288], rcsC (hybrid sensory kinase in two-component regulatory system with RcsB and YojN) [NCBI Gene 916815], pppA (serine/threonine phosphatase) [NCBI Gene 879341], icmF (fused isobutyryl-CoA mutase/GTPase IcmF) [NCBI Gene 7039007], clpV1 (secretion protein ClpV1) [NCBI Gene 879553], trpE (anthranilate synthase component I) [NCBI Gene 879191], trpG (anthranilate synthase component 2) [NCBI Gene 800224], SULT1A1 (sulfotransferase family 1A member 1) [NCBI Gene 6817]
- **Diseases:** cystic fibrosis (MONDO:0009061)
- **Species:** Pseudomonas aeruginosa (taxon 287)

## Full-text entities

- **Diseases:** infection (MESH:D007239), respiratory tract infection (MESH:D012141), CF (MESH:D003550)
- **Chemicals:** cAMP (-), c-di-GMP (MESH:C062025)
- **Species:** Homo sapiens (human, species) [taxon 9606], Pseudomonas aeruginosa (species) [taxon 287]

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12277583/full.md

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Source: https://tomesphere.com/paper/PMC12277583