The nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, a crucial element of innate immunity, plays a pivotal role in immune responses and disease pathogenesis. Dysregulated activation of the NLRP3 inflammasome is strongly linked to the onset of various diseases. Recent studies have demonstrated that the Lactobacillaceae can exert anti-inflammatory effects by regulating the NLRP3 inflammasome activity. Therefore, this review outlines the anti-inflammatory mechanisms by which the Lactobacillaceae regulate the NLRP3 inflammasome activity both directly and indirectly. Additionally, we discuss the roles of specific strains, such as Lactiplantibacillus plantarum, Lacticaseibacillus casei, and Lacticaseibacillus rhamnosus, in intestinal inflammatory diseases, hepatic disorders, neurodegenerative diseases, and metabolic/immune-related conditions. This review aims to lay a foundation for an in-depth investigation of the precise mechanisms underlying the Lactobacillaceae-mediated regulation of the NLRP3 inflammasome and provides novel therapeutic strategies for inflammatory diseases.

Streptococcus pneumoniae is a common opportunistic pathogen that can cause various infectious diseases, including acute otitis media, bronchitis, sinusitis, community-acquired pneumonia, septicemia, and purulent meningitis. Autophagy, a lysosome-dependent intracellular degradation pathway, plays a dual regulatory role in both bacterial infection and host defense against pathogens. During S. pneumoniae infection, host cells can activate xenophagy to eliminate invading bacteria. However, this pathogen has evolved multiple evasion strategies, such as interfering with autophagosome maturation, escaping autophagic encapsulation, and even hijacking the autophagy pathway to promote intracellular survival and dissemination. Recent years have witnessed significant progress in understanding the molecular mechanisms underlying the dynamic interplay between S. pneumoniae and host autophagy systems during bacterial infection, yet a systematic review synthesizing these findings remains unavailable. This review focuses on the interaction network and key mechanisms of S. pneumoniae with host cell autophagy, aiming to provide theoretical foundations and research perspectives for developing novel targeted therapeutic strategies against S. pneumoniae infections.

Bacterial glycoproteins, glycolipids, and polysaccharides are collectively known as glycans, which can serve as pivotal pathogenic factors leading to infection. Bacterial protein glycosylation mainly includes N-glycosylation, O-glycosylation, S-glycosylation, and arginine glycosylation. Glycolipids and polysaccharides are also important glycoconjugates, mainly including lipopolysaccharides, lipoarabinomannan, rhamnolipids, peptidoglycan, teichoic acids, and capsular polysaccharides. Bacterial glycoconjugates can promote host-pathogen interactions, influencing bacterial virulence, drug resistance, and biofilm formation, thereby facilitating bacterial infection. In addition, bacterial glycoconjugates can exert dual effects by modulating the host immune system: on one hand, aiding bacteria in achieving immune evasion and causing host infection; on the other, activating host immunity to help eliminate bacteria and suppress infection. This article provides an overview of bacterial glycans regarding the types, structural characteristics, roles in bacterial adhesion and colonization, and regulation of host immune responses and summarizes the effects of bacterial glycans on infection, aiming to offer a distinct perspective from glycoimmunology and an alternative strategy for clinical prevention and treatment of bacterial infectious diseases.

The spread of antibiotic resistance has made bacterial infections a global public health crisis, posing serious challenges to conventional antibiotic therapy and creating an urgent need to develop novel antibacterial strategies. As viruses are capable of specifically lysing bacteria, phages represent a promising alternative therapeutic strategy due to their unique killing mechanisms and high host specificity. Nevertheless, they face limitations in monotherapy due to their narrow host ranges and the emergence of phage-resistant bacteria. In recent years, phage-antibiotic combination therapy has garnered significant attention. It demonstrates unique advantages in enhancing bactericidal effects, synergistically inhibiting dual-resistance mechanisms, broadening the host range, disrupting biofilms, and treating complex infections. This therapy not only overcomes the limitations of single phage therapy but also paves new avenues for treating multidrug-resistant bacterial infections. This review systematically summarizes the synergistic mechanisms, key influencing factors, current challenges, and optimization strategies of phage-antibiotic combination therapy, aiming to provide a theoretical foundation and practical guidance for further research and clinical translation in this field.

Pseudomonas aeruginosa (PA) is a major cause of hospital-acquired infections. It can survive in a variety of extreme environments, and is highly resistant to antibiotics. PA can attack immunocompromised populations to cause severe infections, being a major cause of mortality in clinical practice. Therefore, rapid diagnosis of PA is critical for infection control. Conventional detection techniques such as plate assays, immunoassays, and nucleic acid assays have excellent accuracy and sensitivity, while they are costly and time-consuming. In recent years, novel biosensing technologies have achieved ultrasensitive and precise detection of PA by integrating various biorecognition elements and signal enhancement strategies, providing an efficient, convenient, and cost-effective solution for the rapid identification, treatment, and control of PA. In this paper, we systematically review the principles, application progress, and challenges of magnetic separation biosensing technologies based on electrochemical, optical, CRISPR/Cas12a system, and magnetic nanoparticles, and provide future research directions, aiming to promote the innovation and clinical application of the technologies for rapid detection of PA.

Mobile genetic elements drive bacterial evolution, while exposing bacteria to the risk of invasion by “selfish genes”. In the arms race with mobile genetic elements, bacteria have evolved a range of immune systems that can protect hosts from invading nucleic acids. These immune systems are capable of preventing the invasion of mobile genetic elements, degrading invading nucleic acids, inhibiting the replication or transcription of invading nucleic acids, or inducing abortive infections to protect the population. Although much is known about the working mechanisms of these host immune systems, it remains unclear how bacteria orchestrate different defense strategies in response to different stages of nucleic acid invasion. Based on our research and different immune strategies of bacteria to limit mobile genetic elements in different spatiotemporal dimensions, this review summarizes and classifies the host immune systems. The elucidation of these multilayered immune mechanisms not only reveals the arms race between host and mobile gene elements in the evolutionary process but also underpins the development of new biotechnologies.

In multicellular organisms, cell death is perpetually in a dynamic process. Apoptosis as a pivotal form of regulated cell death, mainly encompasses two pathways: the intrinsic pathway and the extrinsic pathway. During the pathogen infection, host cells are capable of eliminating the infected cells through apoptosis. On the other hand, pathogens have evolved a multitude of strategies to regulate host cell apoptosis. These strategies involve the use of effector proteins to modulate cellular signaling pathways, the regulation of the expression of apoptosis-related genes, the control of key proteins within the apoptosis pathway, and the modulation of the activity of proteases in the Caspase family. This article provides a comprehensive review of the molecular mechanisms and strategies by which intracellular pathogens, such as viruses, bacteria, parasitic fungi, and parasites, regulate host cell apoptosis. The aim is to offer valuable references for further exploration of the intricate interaction mechanisms between pathogens and hosts.

There are a large number of non-rhizobia endophytes in addition to rhizobia in leguminous root nodules, which are of great significance for promoting plant growth and improving the bacterial abundance in root nodules. Some NREs can not only help rhizobia expand their host range but also participate in the leguminous plant-rhizobia symbiotic nodulation process. In this review, we systematically summarize the genetic diversity, classification, and functions of NREs, specifically describe the pathways of NREs entering rhizobia, the interaction mechanism between NREs and rhizobia, and the diversity of NREs in soil ecosystems, and discuss the application potential and future research directions of NREs. Furthermore, this article summarizes the current research progress in leguminous plant-rhizobia-NREs interactions and explores the methods of improving crop productivity and health through interactions mediated by nodule microecology, aiming to provide theoretical support for sustainable agricultural development.

The potent antibacterial activity of silver nanoparticles is primarily attributed to the release of silver ions, which disrupt cell membranes and inactivate essential enzymes through Ag-S bonding formation. Objective To explore silver ion immobilization to minimize silver release. Methods A macrocyclic cryptand with nitrogen bridgeheads was prepared and subsequently chelated with silver ions to produce Cage silver(I), which was then coordinated with different ratios of sulfonated chitosan (SCS) to form SCS/Cage Ag(I) complexes (SCA1, SCA2, and SCA3). The antioxidant activities of the complexes were assessed by reducing power and 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical and hydrogen peroxide scavenging assays. The antibacterial activities of the complexes were evaluated based on the minimum inhibitory concentrations (MICs) and minimum bactericidal concentrations (MBCs) against Staphylococcus aureus ATCC 6538 and Escherichia coli O157:H7 and the inhibition rate on biofilm formation. Results Cage silver(I) exhibited strong antibacterial activity, with the MIC of 0.015 mg/mL and MBC of 0.031 mg/mL against S. aureus ATCC 6538, and the MIC of 0.031 mg/mL and MBC of 0.120 mg/mL against E. coli O157:H7. Significant antioxidant properties of Cage silver(I) were also observed, as demonstrated by the DPPH free radical scavenging rates of 42.2% and 53.1% at 326 nm and 517 nm, respectively. Cage silver(I) exhibited the highest antibacterial and antioxidant activities, followed by SCA1, SCA2, SCA3, and SCS, because the content of silver ions in Cage silver(I) was 10-fold higher than that in SCA1. The antibacterial and antioxidant activities of SCA1 were better than those of Cage silver(I), which further indicated that the sulfonic groups of SCS may intensely coordinate with silver ions to exert synergistic effects. Conclusion Combining the merits of silver ions and SCS improves the bioavailability of the agent at microbicidal concentrations, minimizes the accumulation in the environment, and reduces treatment costs. The method developed herein offers a sustainable approach to enhance microbial control while minimizing the impact on the environment.

With the development of human industrial activities, nitrogen (N) emissions and atmospheric N deposition have increased significantly. When atmospheric N deposition exceeds the critical load that plants can bear, it may exert a negative effect on plants and lead to a decrease in species abundance. As an important biotic factor affecting species abundance, mycorrhizae can affect plant diversity and community structure through nutrient supply and hyphal network mechanism. Objective To compare the critical load of N deposition of understory herbaceous plants with different mycorrhizal types and explore how mycorrhizal types affect the responses of understory herbaceous plants to N deposition. Methods According to the database of long-term N deposition critical load of forest herbaceous plants, and the published literature, critical load database of herbaceous plants under different mycorrhizal types of forest forests in response to N deposition was established. We identified three mycorrhizal types of forest dominant species, which included arbuscular mycorrhiza (AM), ectomycorrhiza (ECM), and AM+ECM. The effects of mycorrhizal types on the critical load of N deposition of understory herbaceous plants were investigated. Results The critical load of N deposition of understory herbaceous plants varied in forests of different mycorrhizal types (P<0.05). The critical load of N deposition was the highest [9.28 kg N/(ha·a)] in the forest of the AM+ECM type, the second [8.41 kg N/(ha·a)] in the forest of the ECM type, and the lowest [7.19 kg N/(ha·a)] in the forest of the AM type. In forests of different mycorrhizal types, the critical loads of understory herbaceous plants of different functional groups (gramineous and non-gramineous) in response to N precipitation were consistent with the responses of all understory herbaceous plants of different mycorrhizal types. N deposition caused changes in the abundance of understory herbaceous plants. The species abundance of understory herbaceous plants in the forest of the AM type showed an increasing trend, while that in the forest of the ECM type mainly decreased. Conclusion Mycorrhizal types affect the critical load of N deposition of understory herbaceous plants (P<0.05), which is related to the niche differentiation, N concentration of litter, and N acquisition strategies of different mycorrhizal types of plants. In addition, the abundance of understory herbaceous plants will also vary due to different mycorrhizal types.