Co-Regulation Of Fimh, Luxs, And Hlya Genes In E. Coli Isolates Under Chemical Stress: A Study On Cross-Gene Expression Dynamics

Abstract

Antimicrobial treatments, while designed to eradicate bacterial pathogens, can unexpectedly encourage bacterial virulence abilities. This study explored the influence of various antimicrobial agents (Dettol, surgical soap, ciprofloxacin, ceftriaxone, and gentamicin) on the expression of three key virulence genes: hyl (hyaluronidase), fim (fimbrial adhesin), and lux (quorum sensing) in Escherichia coli using quantitative PCR. Clinical samples were collected from Al Ramadi Teaching Hospital and Al Ramadi Teaching Hospital for Gynecology and Pediatrics, during the period between December 2024 to March 2025. Gene expression was standardized using the 2−ΔΔCt method, with fold changes calculated relative to an untreated control. All antimicrobial treatments reliably stimulated the upregulation of these virulence genes, representing complex stress-responsive way activation in bacteria.

The hyl gene, encoding a spreading factor, exhibited consistent upregulation through all treatments, with gentamicin inducing the highest rise (6.45-fold). This proposes that protein synthesis inhibition and oxidative stress may powerfully promote bacterial tissue penetration. The fim gene, serious for adhesion and biofilm formation, exhibited significant upregulation, mainly with ciprofloxacin (8.98-fold) and ceftriaxone (8.79-fold), suggesting that DNA damage and cell wall stress activate enhanced surface association for perseverance. Most strangely, the lux gene, elaborate in quorum sensing, revealed a dramatic 14.44-fold upregulation with ciprofloxacin, emphasizing an unprecedented activation of bacterial communication networks. These results reveal that sub-lethal levels of antimicrobials can trigger integrated stress response systems in bacteria, leading to the corresponding expression of multiple virulence factors. This phenomenon poses a significant challenge to antimicrobial therapy, as treatments intended to eliminate bacteria may inadvertently enhance their pathogenic potential. In conclusions, antimicrobial treatments paradoxically enhance bacterial virulence by upregulating key genes for spreading, adhesion, and communication.