Potential antibacterial effects and transcriptomic analysis of a novel reversible photoacid-based crystalline coordination polymer

Abstract

Introduction: With the increasing prevalence of antibiotic resistance, the development of novel antibacterial materials is crucial to combat clinically relevant pathogens. This study comprehensively investigated the antibacterial properties and underlying mechanisms of a novel reversible photoacid-based crystalline material.

Methods: The antibacterial efficacy of the material was evaluated against six clinically relevant pathogenic bacteria, including multidrug-resistant strains. The inhibition rates were determined, and scanning electron microscopy (SEM) was used to observe the effects on cell surface integrity. Transcriptomic analysis was conducted to elucidate the underlying antibacterial mechanisms.

Results: The material exhibited broad-spectrum antibacterial activity, with higher sensitivity toward Gram-negative bacteria. Blue light irradiation significantly enhanced its antibacterial efficacy. SEM revealed that the material disrupted cell membrane integrity, leading to cell death. Transcriptomic analysis showed that the material inhibited bacterial protein synthesis, disrupted cell membrane protein synthesis, and downregulated oxidative stress-related genes, causing ROS accumulation and inhibiting cell growth.

Discussion: These findings provide a theoretical basis for the potential clinical application of this material as a new antibacterial agent. The material's ability to enhance antibacterial efficacy through light irradiation and its broad-spectrum activity suggest it could be a valuable tool in combating antibiotic-resistant pathogens. Future research should focus on further exploring the antibacterial mechanisms and evaluating the material's safety and efficacy in clinical settings.

Keywords: SEM; clinical pathogens; inhibition rate; photoacid; transcriptomic analysis.

Figure 1

The effects of different treatments on the IR of E. coli. (A) Comparison of photoacid-based crystal materials and simulated PXRD patterns. (B) Blue: blue light irradiation with Compound 1 added; Green: dark conditions with Compound 1 added; Yellow: blue light irradiation with HPTS added. One-way ANOVA–Dunnett test; p < 0.05 (*), p < 0.01 (**) or p < 0.001 (***).

Figure 2

The effect of adding different concentrations of Compound 1 on the IR of six common pathogenic bacteria. (A) E.coli. (B) P. aeruginosa (C). S. aureus (D) B. subtilis. (E) MDR-PA (F). MRSA. Six strains were added with the Compound 1 at concentrations of 0 mg/mL, 0.005 mg/mL, 0.01 mg/mL, 0.025 mg/mL, 0.05 mg/mL, 0.1 mg/mL, 0.25 mg/mL, 0.5 mg/mL, 1.0 mg/mL, and 2.0 mg/mL when they had grown to the logarithmic phase. Then they were incubated 16 h at 37°C under blue light exposure. The IR was determined for each strain at the various concentrations of Compound 1. p > 0.05 (ns), p < 0.05 (*), p < 0.01 (**) or p < 0.001 (***).

Figure 3

The effect of Compound 1 on cell membrane of different strains. SEM images of E. coli, P. aeruginosa, MDR-PA, B. subtilis, S. aureus and MRSA cells after they were the treated with the Compound 1 at a concentration of 0.1 mg/mL, and the control experiment.

Figure 4

Molecular diversity of MRSA following Compound 1 treatment. (A) PCA analysis of RNA sequencing results showing differences in gene expression between control and Compound 1-treated MRSA. (B) Volcano plot showing differentially expressed genes between control and Compound 1-treated MRSA. Significance was defined as padjust<0.05 and |log2(fold change)| > 1. (C) Representative GO terms after Compound 1 treatment. (D) Representative KEGG entries after Compound 1 treatment.

Figure 5

Heatmap showing expression levels of key genes in the control and compound 1-treated groups.