Phthalates Boost Natural Transformation of Extracellular Antibiotic Resistance Genes through Enhancing Bacterial Motility and DNA Environmental Persistence.

The environmental dissemination of extracellular antibiotic resistance genes (eARGs) in wastewater and natural water bodies has aroused growing ecological concerns. The coexisting chemical pollutants in water are known to markedly affect the eARGs transfer behaviors of the environmental microbial community, but the detailed interactions and specific impacts remain elusive so far. Here, we revealed a concentration-dependent impact of dimethyl phthalate (DMP) and several other types of phthalate esters (common water pollutants released from plastics) on the natural transformation of eARGs. The DMP exposure at an environmentally relevant concentration (10 µg/L) resulted in a 4.8-times raised transformation frequency of Acinetobacter baylyi but severely suppressed the transformation at a high concentration (1000 µg/L). The promotion by low-concentration DMP was attributed to multiple mechanisms, including increased bacterial mobility and membrane permeability to facilitate eARGs uptake and improved resistance of the DMP-bounded eARGs (via noncovalent interaction) to enzymatic degradation (with suppressed DNase activity). Similar promoting effects of DMP on the eARGs transformation were also found in real wastewater and biofilm systems. In contrast, higher-concentration DMP suppressed the eARGs transformation by disrupting the DNA structure. Our findings highlight a potentially underestimated eARGs spreading in aquatic environments due to the impacts of coexisting chemical pollutants and deepen our understanding of the risks of biological-chemical combined pollution in wastewater and environmental water bodies.

Optical Tracking of Surfactant-Tuned Bacterial Adhesion: a Single-Cell Imaging Study.

Probing the interfacial dynamics of single bacterial cells in complex environments is crucial for understanding the microbial biofilm formation process and developing antifouling materials, but it remains a challenge. Here, we studied single bacterial interfacial behaviors modulated by surfactants via a plasmonic imaging technique. We quantified the adhesion strength of single bacterial cells by plasmonic measurement of potential energy profiles and dissected the mechanism of surfactant-tuned single bacterial adhesion. The presence of surfactant tuned single bacterial adhesion by increasing the thickness of extracellular polymeric substances (EPS) and reducing the degree of EPS cross-linking. The adhesion kinetics and equilibrium state of bacteria attached to the surface confirmed the decrease in adhesion strength tuned by surfactants. The information obtained is valuable for understanding the interaction mechanism between a single bacterial cell and surface, developing new biofilm control strategies, and designing anticontamination materials. IMPORTANCE Studying the interfacial dynamic of single bacteria in complex environments is crucial for understanding the microbial biofilm formation process and developing antifouling materials. However, quantifying the interactions between microorganisms and surfaces in the presence of pollution at the single-cell level remains a great challenge. This paper presents the analysis of single bacterial interfacial behaviors modulated by surfactants and quantification of the adhesion strength via a plasmonic imaging technique. Our study provided insights into the mechanism of initial bacterial adhesion, facilitating our understanding of the adhesion process at the microscopic scale, and is of great value for controlling membrane fouling biofilm formation.

The Integrated Analysis Identifies Three Critical Genes as Novel Diagnostic Biomarkers Involved in Immune Infiltration in Atherosclerosis.

Atherosclerosis (AS), a chronic inflammatory disease of the blood vessels, is the primary cause of cardiovascular disease, the leading cause of death worldwide. This study aimed to identify possible diagnostic markers for AS and determine their correlation with the infiltration of immune cells in AS. In total, 10 serum samples from AS patients and 10 samples from healthy subjects were collected. The original gene expression profiles of GSE43292 and GSE57691 were downloaded from the Gene Expression Omnibus database. Least absolute shrinkage and selection operator regression model and support vector machine recursive feature elimination analyses were carried out to identify candidate markers. The diagnostic values of the identified biomarkers were determined using receiver operating characteristic assays. The compositional patterns of the 22 types of immune cell fraction in AS were estimated using CIBERSORT. RT-PCR was performed to further determine the expression of the critical genes. This study identified 17 differentially expressed genes (DEGs) in AS samples. The identified DEGs were mainly involved in non-small cell lung carcinoma, pulmonary fibrosis, polycystic ovary syndrome, glucose intolerance, and T-cell leukemia. FHL5, IBSP, and SCRG1 have been identified as the diagnostic genes in AS. The expression of SCRG1 and FHL5 was distinctly downregulated in AS samples, and the expression of IBSP was distinctly upregulated in AS samples, which was further confirmed using our cohort by RT-PCR. Moreover, immune assays revealed that FHL5, IBSP, and SCRG1 were associated with several immune cells, such as CD8 T cells, naïve B cells, macrophage M0, activated memory CD4 T cells, and activated NK cells. Overall, future investigations into the occurrence and molecular mechanisms of AS may benefit from using the genes FHL5, IBSP, and SCRG1 as diagnostic markers for the condition.