Metal-organic frameworks (MOFs), which have become popular in recent years as excellent carriers of drugs and biomimetic materials, have provided new research ideas for fighting pathogenic bacterial infections. Although various antimicrobial metal ions can be added to MOFs with physical methods, such as impregnation, to inhibit bacterial multiplication, this is inefficient and has many problems, such as an uneven distribution of antimicrobial ions in the MOF and the need for the simultaneous addition of large doses of metal ions. Here, we report on the use of MIL-101(Fe)@Ag with efficient metal-ion release and strong antimicrobial efficiency for co-sterilization. Fe-based MIL-101(Fe) was synthesized, and then Ag⁺ was uniformly introduced into the MOF by the substitution of Ag⁺ for Fe³⁺. Scanning electron microscopy, powder X-ray diffraction (PXRD) Fourier transform infrared spectroscopy, and thermogravimetric analysis were used to investigate the synthesized MIL-101(Fe)@Ag. The characteristic peaks of MIL-101(Fe) and silver ions could be clearly seen in the PXRD pattern. Comparing the diffraction peaks of the simulated PXRD patterns clearly showed that MIL-101(Fe) was successfully constructed and silver ions were successfully loaded into MIL-101(Fe) to synthesize an MOF with a bimetallic structure, that is, the target product MIL-101(Fe)@Ag. The antibacterial mechanism of the MOF material was also investigated. MIL-101(Fe)@Ag exhibited low cytotoxicity, so it has potential applications in the biological field. Overall, MIL-101(Fe)@Ag is an easily fabricated structurally engineered nanocomposite with broad-spectrum bactericidal activity.

Metal-Organic Frameworks (MOFs) offer new ideas for the design of antibacterial materials because of their antibacterial properties, high porosity and specific surface area, low toxicity and good biocompatibility compared with other nanomaterials. Herein, a novel antimicrobial nanomaterial, MIL-101(Fe)@ZnO, has been synthesized by hydrothermal synthesis and characterized by FTIR, UV-vis, ICP-OES, XRD, SEM, EDS and BET to show that the zinc ions are doped into the crystal lattice of MIL-101(Fe) to form a Fe-Zn bimetallic structure. MIL-101(Fe)@ZnO was found to be effective against a wide range of antibacterial materials including Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Acinetobacter baumannii, Acinetobacter junii and Staphylococcus epidermidis. It has a significant antibacterial effect, weak cytotoxicity, high safety performance and good biocompatibility. Meanwhile, MIL-101(Fe)@ZnO was able to achieve antibacterial effects by causing cells to produce ROS, disrupting the cell membrane structure, and causing protein leakage and lipid preoxidation mechanisms. In conclusion, MIL-101(Fe)@ZnO is an easy-to-prepare antimicrobial nanomaterial with broad-spectrum bactericidal activity and low toxicity.

Nanomaterial technology has attracted much attention because of its antibacterial and drug delivery properties, among other applications. Metal-organic frameworks (MOFs) have advantages, such as their pore structure, large specific surface area, open metal sites, and chemical stability, over other nanomaterials, enabling better drug encapsulation and adsorption. In two examples, we used the common pathogenic bacterium Staphylococcus aureus and highly infectious influenza A virus. A novel complex MIL-101(Fe)-T705 was formed by synthesizing MOF material MIL-101(Fe) with the drug favipiravir (T-705), and a hot solvent synthesis method was applied to investigate the in vitro antibacterial and antiviral activities. The results showed that MIL-101(Fe)-T705 combined the advantages of nanomaterials and drugs and could inhibit the growth of Staphylococcus aureus at a concentration of 0.0032 g/mL. Regarding the inhibition of influenza A virus, MIL-101(Fe)-T705 showed good biosafety at 12, 24, 48, and 72 h in addition to a good antiviral effect at concentrations of 0.1, 0.2, 0.4, 0.8, 1.6, and 3 μg/mL, which were higher than MIL-101(Fe) and T-705.

Air purifiers should pay much attention to hospital-associated infections, but the role of a single air purifier is limited. The goal of this study was to evaluate the effectiveness of the combined application of the nonequilibrium positive and negative oxygen ion purifier (PNOI) and the high-efficiency particulate air filter (HEPA) on a complex, polluted environment. Two of the better performing purifiers were selected before the study. The efficacy of their use alone and in combination for purification of cigarette particulate matter (PM), Staphylococcus albicans, and influenza virus were then evaluated under a simulated contaminated ward. PNAI and HEPA alone are deficient. However, when they were combined, they achieved 98.44%, 99.75%, and 100% 30 min purification rates for cigarette PM, S. albus, and influenza virus, respectively. The purification of pollution of various particle sizes and positions was optimized and reduced differentials, and a subset of airborne influenza viruses is inactivated. Furthermore, they were superior to ultraviolet disinfection for microbial purification in air. This work demonstrates the strong purification capability of the combined application of these two air purifiers for complex air pollution, which provides a new idea for infection control in medical institutions.

The exacerbation of pneumonia in children with human adenovirus type 3 (HAdV-3E) is secondary to a Staphylococcus aureus (S. aureus) infection. The influence of host–pathogen interactions on disease progression remains unclear. It is important to note that S. aureus infections following an HAdV-3E infection are frequently observed in clinical settings, yet the underlying susceptibility mechanisms are not fully understood. This study utilized an A549 cell model to investigate secondary infection with S. aureus following an HAdV-3E infection. The findings suggest that HAdV-3E exacerbates the S. aureus infection by intensifying lung epithelial cell damage. The results highlight the role of HAdV-3E in enhancing the interferon signaling pathway through RIG-I (DDX58), resulting in the increased expression of interferon-stimulating factors like MX1, RSAD2, and USP18. The increase in interferon-stimulating factors inhibits the NF-κB and MAPK/P38 pro-inflammatory signaling pathways. These findings reveal new mechanisms of action for HAdV-3E and S. aureus in secondary infections, enhancing our comprehension of pathogenesis.