Around the globe, surges of bacterial diseases are causing serious health threats and related concerns. Recently, the metal ion release and photodynamic and photothermal effects of nanomaterials were demonstrated to have substantial efficiency in eliminating resistance and surges of bacteria. Nanomaterials with characteristics such as surface plasmonic resonance, photocatalysis, structural complexities, and optical features have been utilized to control metal ion release, generate reactive oxygen species, and produce heat for antibacterial applications. The superior characteristics of nanomaterials present an opportunity to explore and enhance their antibacterial activities leading to clinical applications. In this review, we comprehensively list three different antibacterial mechanisms of metal ion release, photodynamic therapy, and photothermal therapy based on nanomaterials. These three different antibacterial mechanisms are divided into their respective subgroups in accordance with recent achievements, showcasing prospective challenges and opportunities in clinical, environmental, and related fields.

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An upsurge in the multidrug-resistant (MDR) bacterial pestilence is a global cause for concern in terms of human health. Lately, nanomaterials with photothermal effects have assisted in the efficient killing of MDR bacteria, attributable to their uncommon plasmonic, photocatalytic, and structural properties. Examinations of substantial amounts of photothermally enabled nanomaterials have shown bactericidal effects in an optimized time under near-infrared (NIR) light irradiation. In this review, we have compiled recent advances in photothermally enabled nanomaterials for antibacterial activities and their mechanisms. Photothermally enabled nanomaterials are classified into three groups, including metal-, carbon-, and polymer-based nanomaterials. Based on substantial accomplishments with photothermally enabled nanomaterials, we have inferred current trends and their prospective clinical applications.

The metallic phase of 1T-MoS2 nanoflowers (NFs) and the semiconducting phase of 2H-MoS2 NFs were prepared by a facile solvothermal and combustion method. The antibacterial activities, reactive oxygen species (ROS) generation, and light-driven antibacterial mechanism of metallic 1T-MoS2 NFs and semiconducting 2H-MoS2 NFs were demonstrated with the bacterium Escherichia coli (E. coli) under light irradiation. Results of the bacterial growth curve and ROS generation analyses revealed higher light-driven antibacterial activity of metallic 1T-MoS2 NFs compared to semiconducting 2H-MoS2 NFs. Electron paramagnetic resonance (EPR) spectroscopy demonstrated that the ROS of the superoxide anion radical •O2 – was generated due to the incubation of 1T-MoS2 NFs and E. coli with light irradiation. Furthermore, E. coli incubated with metallic 1T-MoS2 NFs exhibited significant damage to the bacterial cell walls, complete bacterial destruction, and abnormal elongation after light irradiation. The light-driven antibacterial mechanism of metallic 1T-MoS2 NFs was examined, and we found that, under light irradiation, photoinduced electrons were generated by metallic 1T-MoS2 NFs, and then the photoinduced electrons reacted with oxygen to generate superoxide anion radical which induced bacterial death. For semiconducting 2H-MoS2 NFs, photoinduced electrons and holes rapidly recombined resulting in a decrease in ROS generation which diminished the light-driven antibacterial activity.

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Interferon (IFN)-γ is crucial for normal immune surveillance and exhibits immunomodulatory, antimicrobial, and anticancer activity. Patients with nontuberculous mycobacteria (NTM) infection commonly express high levels of anti-IFN-γ autoantibodies (autoAbs) and suffer from recurrent infections due to adult-onset immunodeficiency with defects in IFN-γ immune surveillance. In this study, we developed the methods for determination of anti-IFN-γ autoAbs and then characterized their neutralizing activity in patients with NTM infection. A modified sandwich ELISA-based colorimetric assay followed by immunoblot analysis detected the presence of autoAbs in three out of five serum samples. Serum levels of IFN-γ were decreased. Synthetic peptide binding assay showed variable patterns of epitope recognition in patients positive for anti-IFN-γ autoAbs. Functional tests confirmed that patient serum blocked IFN-γ-activated STAT1 activation and IRF1 transactivation. Furthermore, IFN-γ-regulated inflammation, chemokine production and cytokine production were also blocked. These results provide potentially useful methods to assay anti-IFN-γ autoAbs and to characterize the effects of neutralizing autoAbs on IFN-γ signaling and bioactivity.

An outbreak of a bacterial contagion is a critical threat for human health worldwide. Recently, light-activated heterostructured nanomaterials (LAHNs) have shown potential as antibacterial agents, owing to their unique structural and optical properties. Many investigations have revealed that heterostructured nanomaterials are potential antibacterial agents under light irradiation. In this review, we summarize recent developments of light-activated antibacterial agents using heterostructured nanomaterials and specifically categorized those agents based on their various light harvesters. The detailed antibacterial mechanisms are also addressed. With the achievements of LAHNs as antibacterial agents, we further discuss the challenges and opportunities for their future clinical applications.

The interferon- (IFN-) γ expression is elicited in response to microbial infections and activates immune surveillance by antimicrobial immune elements to induce microbial killing. Patients with adult-onset immunodeficiency who suffer from recurrent infections with microbes, particularly nontuberculous mycobacteria (NTM), commonly display genetic defects in IFN-γ signaling as well as the generation of anti-IFN-γ autoantibodies (autoAbs). Because IFN-γ is an activator of macrophage differentiation and a proinflammatory activator of innate immunity, the blockade effects of the autoAbs present in NTM patient serum on IFN-γ are hypothesized to regulate the antimicrobial function of macrophages. In the presence of patient serum, IFN-γ-induced type 1 macrophage (M1) differentiation was inhibited in PMA-stimulated human monocytic THP-1 cells. Treatment with patient serum significantly blocked the production of proinflammatory factors, including cytokines/chemokines and reactive oxygen/nitrogen species, by M1 macrophages. Importantly, IFN-γ-facilitated phagocytosis and degradation of heat-killed mycobacterium were decreased by cotreatment with patient serum. These results show the blockade activity of anti-IFN-γ autoAbs on IFN-γ-mediated antimicrobial immunity in macrophages.