The elimination of biofilms is a crucial step in controlling hospital-acquired infections.Once biofilms colonize luminal instruments,it is difficult to remove them using traditional disinfection methods.Conventional disinfection approaches now face a series of challenges,including microbial resistance,corrosiveness,cytotoxicity,residual disinfection byproducts,and environmental pollution.Therefore,developing novel disinfection technologies specifically targeting biofilm removal is vitally important.New disinfection technologies,such as slightly acidic electrolyzed water,plasma technology,surface modification techniques,nanomaterial-based disinfection,bacteriophage disinfection,and enzymatic disinfection,are constantly emerging.These technologies exhibit excellent performance against biofilms by leveraging the synergistic effects of multiple mechanisms,including the reactive oxygen species(ROS)burst,photocatalytic oxidation,physical disruption,and biological targeting.This review summarizes the characteristics,underlying mechanisms,and potential application scenarios of these novel disinfection technologies,with a particular focus on their effects against biofilms formed by common pathogenic bacteria on surfaces in hospital settings.It aims to provide a reference basis for the practical application and translation of these disinfection technologies and the development of new disinfection strategies.

Objectives:To investigate the genetic characteristics of the blaNDM-1-carrying plasmid of the multidrug resistant Enterobacter hormaechei subsp. hoffmannii clinical isolate C37, and constructing a phylogenetic tree of the 66 publicly available genomes of the Enterobacter hormaechei subsp. hoffmannii to explore its global epidemic situation. Methods:Carbapenem-resistant Enterobacter cloacae complex (CRECC) strains isolated from the First Affiliated Hospital of Sun Yat-sen University from August 2014 to August 2021 were collected. Matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) and 16S rDNA Sanger sequencing were used for species identification. Micro broth dilution method was used for antibacterial susceptibility test. The polymerase chain reaction (PCR) was used to detect the β-lactamase resistance gene and plasmid-mediated quinolone resistance (PMQR) gene carried by the C37 strain. The conjugation experiment was used to confirm the conjugative metastasis of the resistance genes in C37 strain. Whole genome of the C37 strain was sequenced. Core genome was extracted and the phylogenetic analysis of 66 publicly available Enterobacter hormaechei subsp. hoffmannii was performed. Results:Enterobacter hormaechei subsp. hoffmannii C37 strain is resistant to third-generation cephalosporins, carbapenems, aminoglycosides and quinolones, and carries blaACT-5, blaNDM-1, qnrA1, aac(6′)-Ib-cr, oqxAB, fosA, dfrA15 and other resistance genes, as well as IncX3, IncX4, IncFIB and IncFII plasmids. Multilocus sequence typing (MLST) analysis showed that C37 strain belongs to the ST78 type of Enterobacter cloacae complex (ECC). Conclusions:ST78 type Enterobacter hormaechei subsp. hoffmannii is closely related to the spread of carbapenem resistance genes. It is a potential high-risk clone to spread carbapenem resistance genes. The prevalence and trends of ST78 type Enterobacter hormaechei subsp. Hoffmannii should be monitored.

Objective To explore the effect and mechanism of hesperidin in treating the lung injury in the mouse model of respiratory syncytial virus (RSV)-induced bronchiolitis. Methods A mouse model of RSV-induced bronchiolitis was established,and 60 BALB/c mice were assigned into a control group,a model group,a low-dose hesperidin (18 mg/kg) group,a high-dose hesperidin (36 mg/kg) group,and a high-dose hesperidin (36 mg/kg)+Jagged1(1 mg/kg) group by random number table method,with 12 mice in each group. Corresponding doses of drugs were administrated for intervention,and the control group and model group were administrated with the same amount of saline.The bronchoalveolar lavage fluid (BALF) samples were collected and alveolar macrophages were isolated.ELISA was employed to detect the levels of interleukin (IL)-4,IL-6,tumor necrosis factor-α (TNF-α),and IL-10 in BALF,and flow cytometry to detect the M1/M2 polarization of macrophages.qRT-PCR and Western blotting were respectively conducted to detect the mRNA and protein levels of inducible nitric oxide synthase (iNOS),arginase 1 (Arg-1),Jagged1,and Notch1 in the lung tissue. Results Compared with the control group,the modeling of RSV-induced bronchiolitis elevated the IL-4,IL-6,and TNF-α levels,increased the proportion of M1-type macrophages and the lung inflammation and mucus secretion scores,and up-regulated the mRNA and protein levels of iNOS,Jagged1,and Notch1 in BALF (all P<0.001).Meanwhile,the modeling lowered the IL-10 level,decreased the proportion of M2-type macrophages,and down-regulated the mRNA and protein levels of Arg-1 (all P<0.001).Compared with the model group,low- and high-dose hesperidin lowered the IL-4,IL-6,TNF-α levels,decreased the proportion of M1-type macrophages and the lung inflammation and mucus secretion scores,and down-regulated the mRNA and protein levels of iNOS,Jagged1,and Notch1 in BALF (all P<0.05).Moreover,hesperidin elevated the IL-10 level,increased the proportion of M2-type macrophages,and up-regulated the mRNA and protein levels of Arg-1 (all P<0.001).Using recombinant Jagged1 protein to activate Notch1 signaling pathway can significantly attenuate the promotion of high-dose hesperidin on M2 macrophage polarization and amelioration of lung inflammation damage (all P<0.01). Conclusion Hesperidin may alleviate the lung inflammation damage in mice with RSV-induced bronchiolitis by inhibiting the Jagged1/Notch1 signaling pathway and promoting the M2-type polarization of macrophages.
Animals ; Mice ; Bronchiolitis/metabolism* ; Hesperidin/metabolism* ; Interleukin-10/pharmacology* ; Interleukin-4/pharmacology* ; Interleukin-6/metabolism* ; Jagged-1 Protein/pharmacology* ; Lung Injury/metabolism* ; Macrophages ; Mice, Inbred BALB C ; RNA, Messenger/metabolism* ; Tumor Necrosis Factor-alpha/metabolism*