ABSTRACT Chlorogenic acid (CGA) aids diabetic wound healing via antioxidant, antibacterial, and pro‐migration effects, but poor stability and low membrane permeability limit its use in chronic diabetes. Therefore, we employed a one‐pot method to mix naphthalene‐modified diphenylalanine (FF) and hyaluronic acid (HA) to prepare an injectable composite hydrogel capable of delivering CGA to inflamed wounds and enabling sustained‐release drug delivery, thereby promoting the healing of diabetic wounds. We evaluated it through the rheological and morphological properties, as well as the in vitro biocompatibility of the hydrogel. Structurally, the hydrogel exhibits a uniform nanofiber network, conferring enhanced mechanical strength and stable drug‐loading capacity. In a mouse wound model, it reduced wound area to 7.99% ± 0.73% after 12 days of treatment, with increased granulation tissue, collagen deposition, and microvascular density compared with the normal saline group. Collectively, these findings indicate that the peptide‐based composite hydrogel promotes local angiogenesis and vascular maturation, thereby accelerating the healing process of chronic diabetic wounds. This system represents a promising strategy for the development of bioactive wound dressings. Nevertheless, the underlying molecular mechanisms remain to be fully elucidated, and further validation in large animal models is required prior to clinical translation.

Introduction Chinese herbal medicine offers a multi-target approach to modulate key immune signaling pathways, yet its clinical translation remains underexplored. Periodontitis is a plaque biofilm-induced chronic inflammatory disease causing immune imbalance and periodontal tissue destruction. Drug resistance and systemic toxicity limit the use of conventional treatments. This review focuses on the clinical relevance of Chinese herbal medicine in regulating core signaling pathways, including nuclear factor kappa B (NF-κB), mitogen‑activated protein kinase (MAPK), and phosphatidylinositol 3-kinase / protein kinase B (PI3K/Akt), thereby providing a mechanistic and therapeutic perspective on its role in periodontitis and highlighting its therapeutic potential. Methods Recently published articles were reviewed by searching combinations of keywords in PubMed, Google Scholar and other databases (inception to 2025), including ‘periodontitis’, ‘Chinese herbal medicine’, ‘immune regulation’, ‘osteoclast’, ‘signaling pathway’ and specific botanical names. We focused on the regulatory effects of Chinese herbal medicine bioactive components and formulations on key pathological processes in periodontitis. Of 5,600 initially identified articles, 500 full texts were screened for relevance, and 75 were selected. Results This review investigated the pharmacological properties of the bioactive compounds of Chinese herbal medicine, which inhibit inflammation and apoptosis through multi-target mechanisms. These compounds, such as berberine, resveratrol, and curcumin, can significantly modulate NF-κB, MAPK, and PI3K/Akt signaling pathways. They can attenuate cytokine release, rebalance macrophage polarization, inhibit osteoclastogenesis, and promote osteogenic differentiation. Several Chinese herbal formulations showed synergistic effects when combined with conventional periodontal therapy, improving gingival inflammation, alveolar bone preservation, and symptoms. Discussion The combination of Chinese and Western medicine provides a low-toxicity, high-efficacy therapeutic strategy through multi-dimensional regulation of immune-inflammatory networks and bone homeostasis. This review discusses natural active components and integrates Chinese herbal medicine with modern medicine to promote the clinical transformation of Chinese herb, advancing personalized and precision medicine in periodontitis.

ABSTRACT Tuberculosis (TB) remains a critical global health challenge, associated with significant morbidity and mortality. Traditional therapeutic regimens have largely remained unchanged for decades, but their effectiveness has decreased due to the emergence of drug‐resistant Mycobacterium tuberculosis strains. This rise in drug resistance complicates disease management and facilitates further transmission, highlighting the urgent need for novel and effective therapeutic agents. Traditional Chinese herbal medicines have shown promise in TB treatment by enhancing host immunity, inhibiting drug‐resistant strains of Mycobacterium tuberculosis , and reducing inflammation. However, there is currently no comprehensive and systematic review detailing the specific active ingredients of these herbal medicines and their mechanisms against TB. This paper focuses on four medicinal herbs, Astragalus membranaceus , Forsythia suspensa , Hedyotis diffusa , and Ganoderma lucidum , which contain bioactive compounds with significant anti‐TB properties. We systematically analyze current research to elucidate how these active substances inhibit Mycobacterium tuberculosis growth and modulate host immune responses. The review aims to provide insights that could inform the development of herbal‐based anti‐TB therapies and proposes future research directions to enhance the rational design and clinical application of traditional Chinese medicine (TCM) in TB treatment.

Tuberculosis (TB) remains one of the deadliest infectious diseases worldwide. The substantial reservoir of latent infections, the emergence of multidrug-resistant and extensively drug-resistant TB (MDR/XDR-TB), and the prolonged duration and toxicity of current therapeutic regimens underscore the urgent need for novel treatment strategies. Therapeutic vaccines, an innovative immunotherapeutic approach, are designed to be administered alongside standard pharmacological treatments. By enhancing pathogen-specific immune responses in the host, these vaccines aim to eradicate persistent bacteria, reduce treatment duration, and prevent disease recurrence, thus representing a promising strategy for addressing MDR-TB. This review systematically summarizes the leading therapeutic vaccine candidates currently in clinical trials, detailing the associated mechanisms of action and preclinical and clinical efficacy data. Additionally, the review critically examines existing challenges and outlines future research directions. Overall, this comprehensive analysis seeks to enhance understanding of the potential and development pathways of therapeutic vaccines for TB treatment, contributing to the global effort against this widespread health threat.

Bacillus subtilis (B. subtilis), a versatile microorganism widely applied in agriculture and animal husbandry, has significant potential for supporting food security through crop protection and livestock productivity. On the basis of genomic and in vitro evidence, this study characterized a novel B. subtilis strain, G01, highlighting its potential as a candidate for biological control and food probiotics. Whole-genome sequencing revealed that G01 harbors nine secondary metabolite biosynthesis gene clusters, which play crucial roles in the biological control of microbial pathogens. Crucially, for potential food and feed-related uses, in vitro assays confirmed the potent broad-spectrum antimicrobial activity of G01 against phytopathogens and zoonotic bacteria, in addition to its ability to efficiently hydrolyze proteins and cellulose. Comparative genomics revealed unique gene clusters associated with antibacterial and probiotic-related functions in G01. Furthermore, genes involved in quorum sensing, biofilm formation, and spore production provide genomic support for its environmental resilience - a key characteristic for candidate biocontrol agents and probiotic precursors that target sustainable crop protection and livestock gut health management. This comprehensive genomic and in vitro functional analysis positions B. subtilis G01 as a promising candidate strain with theoretical potential for enhancing safety and efficiency in agricultural and livestock applications, laying a foundation for future in vivo validation of its practical efficacy.

BACKGROUND:Bacillus Calmette-Guérin (BCG) is the only vaccine for tuberculosis (TB) and remains the most effective means of prevention; however, its effectiveness in humans is highly variable with unknown mechanism. METHODS:Using microbiota transplantation and multi-omics strategies (16S rRNA sequencing, metabolomics, proteomics) in mouse models, we investigated the effect of pre-vaccination gut microbiota composition on BCG vaccine efficacy. Furthermore, key findings were validated in human datasets. FINDINGS:Baseline abundance of gut microbiota, especially Akkermansia muciniphila, significantly affects BCG vaccine efficacy. Increasing the baseline levels of A. muciniphila in the gut before vaccination reduced the BCG vaccine responses, resulting in impaired protection against Mycobacterium tuberculosis (Mtb) infection in mice. A. muciniphila-contributed gut co-metabolite palmitoleic acid inhibits the vaccine responses of BCG. Palmitoleic acid acts on vaccine response through the mediation of effector protein MptpB of BCG and identified that MptpB-mediated inhibition of actin cytoskeleton remodelling to activate BCG vaccine responses is required for palmitoleic acid to regulate the efficacy of BCG vaccination. Inhibition of MptpB or actin cytoskeleton remodelling blocks the effects of higher baseline abundance of A. muciniphila on the efficacy of BCG vaccination. Analyses of human datasets provided hypothesis-generating support for these findings. Mechanistically, the higher baseline levels of gut A. muciniphila and its metabolite palmitoleic acid inhibit BCG vaccine efficacy by suppressing MptpB-mediated actin cytoskeleton remodelling. INTERPRETATION:These results show that pre-vaccination differences in gut microbiota composition are a factor accounting for high variation in vaccine effectiveness. Stratifying by baseline gut microbiota profile and metabolism may represent a strategy to enhance future vaccine efficacy. FUNDING:Guang Dong Cheung Kong Philanthropy Foundation, Guangzhou key R & D project, National Natural Science Foundation of China, Key laboratory start-up project (Sixth Affiliated Hospital of Sun Yat-sen University), Guangdong Basic and Applied Basic Research Foundation, Guangzhou Basic and Applied Basic Research Foundation, Doctoral Initial Funding of Guangdong Medical University, Shenzhen Medical Research Fund, Discipline construction project of Guangdong Medical University, Project of Songshan Lake Innovation Center of Medicine & Engineering of Guangdong Medical University.

Immune evasion by Mycobacterium tuberculosis (Mtb) complicates tuberculosis (TB) therapy. Ferroptosis, an iron-dependent form of regulated cell death, is increasingly recognized as a critical process in host-pathogen interactions. We aimed to define the role of poly(C)-binding protein 1 (PCBP1) in macrophage ferroptosis during Mtb infection and to develop a targeted RNA activation (RNAa) nanotherapy to exploit this pathway. We analyzed clinical samples from TB patients and investigated Mtb-host interactions in macrophage models using molecular and biochemical assays. Mannosylated lipid nanoparticles (MLNPs) were engineered to deliver PCBP1-targeting small activating RNAs (saRNAs). Therapeutic efficacy, lung-specific delivery, and biocompatibility were evaluated in a murine TB model. Mtb utilizes the host E3 ubiquitin ligase Trim21 to mediate the proteasomal degradation of PCBP1. PCBP1 loss induced macrophage ferroptosis by modulating its downstream targets GPX4, PTGS2, and HMOX1, promoting bacterial survival. In vitro, saPCBP1@MLNPs restored PCBP1 expression, reversed ferroptosis markers (Fe²⁺, 4-HNE), and reduced Mtb burden. In murine models, the nanotherapy achieved lung-specific delivery, significantly attenuated lung pathology, and enhanced bacterial clearance. PCBP1 is a critical, druggable immune-metabolic checkpoint that governs macrophage ferroptosis in TB. Our targeted RNAa nanotherapy represents a promising host-directed strategy for Mtb infection, linking a key molecular mechanism to a translational therapeutic platform and offering a new approach for treating drug-resistant TB.

Next-generation biomedical tools require antibodies that are specific, stable, and scalable. Immunoglobulin Y (IgY), derived from egg yolk, offers distinct advantages over mammalian IgG, including higher thermal and proteolytic stability, reduced nonspecific binding in mammalian sera, and lower production costs. This review examines IgY as a versatile biorecognition platform and highlights three engineering strategies—nano-conjugation, surface immobilization, and encapsulation—that further expand its diagnostic and therapeutic applications. In diagnostic applications, IgY reduces background interference by ≥ 90

The prevalence of diabetes mellitus (DM) and tuberculosis (TB) comorbidity is constantly rising worldwide, thus there is an urgent need for a co-diagnostic method of TB-DM in the clinic. Here, we introduced a bilateral surface-enhanced Raman scattering (SERS)-microneedle (MN) patch that incorporated Au hybrid mesoporous polydopamine-coated urchin Au/Ag (U@mP@Au) for analyzing glucose in interstitial fluid (ISF) and TB biomarker (ESAT-6/CFP-10) in sputum toward the co-detection of TB-DM comorbidity. The feasibility of the bilateral SERS-MN patch was demonstrated in ex vivo artificial skin, in vivo mouse models, and trials of recruiting patients. In the clinical assessment, DM patients (N = 18) and healthy subjects (N = 3) were classified with satisfactory sensitivity (88.9%) and specificity (100%), among which one DM positive sample (P11) with TB infection was successfully identified. Results revealed the sensitivity (87.5%) and specificity (90.9%) of SERS-MN array for TB diagnosis (N = 33), which were comparable to traditional clinical methods (smear, TST, and Xpert). More importantly, three TB-positive patients (P9, P15, and P20) showed abnormally elevated glucose levels, which is highly suggestive of TB-DM complication. This integrated dual-analyte detecting platform represented a significant step toward the cooperative diagnosis of TB-DM comorbidity, facilitating the early detection of complications by clinicians.

ABSTRACT Rapid and sensitive diagnostic strategies are crucial for the prevention and control of tuberculosis (TB). Unlike the invasive TB diagnostic strategy in the clinic, here we introduce a convenient, portable, and non‐invasive system that is constructed by Ag@Au nanoflower (NF) array‐based sensing facemask and catalytic/plasmonic urchin‐shaped Au─Ag embedded covalent organic framework (U@COF) sensor. This system detects TB antigen ESAT‐6/CFP‐10 complex in droplet or sputum samples from a variety of clinical settings. Practical analysis of clinical samples demonstrates this assay is capable of classifying the negative (N = 12) and positive (N = 17) TB patients with satisfactory sensitivity (76.5%) and specificity (100%), among whom two TB‐infected patients (TB3 and TB5) missed by droplet analysis are successfully identified by sputum analysis. More importantly, two cases with abnormally elevated ESAT‐6/CFP‐10 levels are screened out from close contacts of TB patients (N = 6), which is highly suggestive of TB infection (Close contacts 3 and 4). This portable mask is suitable for rapid diagnosis of TB infection in patients with cough, particularly for screening of TB close contacts.

Tuberculosis (TB), a chronic infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis ), is primarily airborne and remains a global health problem, especially in resource-limited countries and regions. The emergence of drug resistance in M. tuberculosis has rendered the existing means ineffective in the treatment of TB. Therefore, research in new therapeutic directions has become imperative. In this review, we outline functional peptides in terms of the mechanisms of action, anti-TB attempts, advantages and disadvantages, and latest advances, aiming to analyze the research progress in anti-TB peptides.

Tuberculosis (TB) remains the leading cause of death from a single pathogen despite global preventive and control initiatives. Effective control of the TB epidemic remains an urgent concern, necessitating the development of novel strategies for rapid and sensitive TB diagnosis. Current diagnostic methodologies for detecting Mycobacterium tuberculosis (Mtb) infections or diagnosing TB, both conventional and contemporary, are constrained by significant limitations. Nanomaterials have attracted substantial attention in recent decades as prospective candidates for disease therapy and diagnosis, and their unique physicochemical and optical features have shown rising potential for innovative TB diagnostic development. This review systematically summarizes the application of nanotechnology in Mtb detection and TB diagnosis and discusses its advantages, limitations, and challenges, which are expected to enhance the current understanding of innovative technological exploration to counter the trend of TB resurgence.

Rapid and sensitive detection of pathogenic lipopolysaccharide (LPS) is of the utmost importance in pharmaceutical products and food safety. Herein, we presented catalyzed hairpin assembly (CHA)-mediated magnetic/ plasmonic satellite nanoassemblies, made of ternary metallic Au@AgPt-coated metal-organic framework (MOF) nanohybrids (Au@AgPt@MOF) with dual-enhancement SERS output and Au magnetic nanoparticles (AuMNPs) with magnetic enrichment and SERS amplification, for ultrasensitive sensing LPS in pharmaceutical injections. Target LPS initiated aptamer (Apt)-based chain replacement reaction, thereby activating downstream CHA for inducing the aggregation of large satellite nanoassemblies and the amplification of catalytic/SERS signals. Under the optimal condition, this method exhibited good linear response in the range of 10-5-103 ng/mL, with an ultralow limit of detection (LOD) in SERS model (8 fg/mL) and catalytic colorimetric model (56 fg/mL). The selectivity and sensitivity of oligonucleotide-driven signal amplification was validated by in vitro experiments and trials of glucose, troxerutin, lidocaine hydrochloride injection samples. The assay results were closely aligning with those of the standard endotoxin quantitative kit, demonstrating the reliability and availability of this assay. Overall, by incorporating the merits of dual-SERS enhancement of Au@AgPt@MOF substrate, magnetic-meditated satellite strategy, and CHA-cascade amplification response, this platform opened up new opportunities for inspecting LPS in drug injection samples.

Lysine-targeting reversible covalent inhibitors, particularly salicylaldehyde-based compounds such as the Food and Drug Administration (FDA)-approved drug Voxelotor, exhibit significant therapeutic potential but are limited by challenges including instability and off-target effects. To overcome these limitations in kinase inhibitor A5, we devised a pH-responsive prodrug strategy by masking its reactive aldehyde group with an acid-labile hydrazone linkage and enhancing intracellular delivery through conjugation with FK506. The optimized prodrug demonstrated robust antitumor efficacy in K562 tumor-bearing mice. Furthermore, the incorporation of the photosensitizer chlorin e6 (Ce6) led to the formation of self-assembled nanoparticles (AKNP), which not only improved physiological stability and prolonged tumor retention but also enabled light-triggered release of A5 in conjunction with photodynamic therapy (PDT). Our study thus presents a promising prodrug self-assembly strategy that combines the on-demand release of a novel lysine-targeting, reversible covalent kinase inhibitor with PDT in clinical cancer therapy.

Tuberculosis (TB), induced by Mycobacterium tuberculosis (Mtb) infection, remains one of the top killers among infectious diseases. The pathogenesis hallmarks for TB are complex immune escape mechanisms of Mtb and low targeting effects of anti-TB drugs. cGAS signaling, which is responsible for triggering host antibacterial immunity against Mtb infection, has shown potentials to serve as targets for anti-TB immunotherapy. As cGAS agonist manganese ions (Mn2+) can activate cGAS-mediated autophagy to inhibit intracellular Mtb in macrophages, we constructed a functional nanoagonist targeting cGAS signaling based on manganese dioxide nanoparticles, naming Tuf-Rif@HA-MnO2 NPs, for synergistic macrophage-targeted drug delivery and anti-TB immuno-therapeutics. Tuf-Rif@HA-MnO2 NPs can actively target macrophages for rifampicin delivery and react with intracellular glutathione (GSH) to release Mn2+ for cGAS-STING signaling activation, which further promote autophagy and antibacterial M1 polarization of Mtb infected macrophages to achieve synergistic intracellular Mtb clearance. Furthermore, Tuf-Rif@HA-MnO2 NPs can potentiate dendritic cell maturation, CD4+ Th1 cell and CD8+ cytotoxic T cell activation in vivo, which collectively attribute to reduced Mtb burdens and alleviated tissue inflammations in lung of Mtb-infected mice without systemic toxicity. This macrophage targeted drug delivery nanoagonist system is expected to develop rational immunotherapy strategy targeting cGAS signaling against TB and drug-resistant TB. STATEMENT OF SIGNIFICANCE: cGAS-mediated autophagy plays a critical role in Mtb clearance in macrophages. Tuf-Rif@HA-MnO2 NPs specifically deliver rifampicin into macrophage for Mtb clearance. Tuf-Rif@HA-MnO2 NPs activate cGAS-mediated macrophage autophagy for Mtb clearance. Tuf-Rif@HA-MnO2 NPs synergize cGAS-mediated immunotherapy with targeted drug delivery for more effective anti-TB treatment.

Diabetic infections/wounds remain to be a threatening challenge as it seriously leads to lower limb amputation with endless pains and subsequent high economic/psychosocial costs. The exceptional peroxidase-like activity of single-atom nanozymes (SAzymes) holds great promise for chemodynamic therapy (CDT) of diabetic infection, but is extremely restricted by the near-neutral pH and insufficient H2O2 levels in physiological conditions. Herein, we innovated a hollow mesoporous molybdenum single-atom nanozyme (HMMo-zyme) featured with catalytic activity, photothermal performance and drug delivery properties for more effective antibacterial therapeutic in diabetic conditions. The glucose oxidase (GOx) was encapsulated into HMMo-zyme with phase-change material (PCM) to form HMMo/GOx@P system, which could be controllably disassembled by near-infrared ray (NIR) to trigger cascade CDT toward bacterial infections. The results revealed that the release of GOx accelerated by NIR could facilitate the continuous conversion of glucose (Glu) into gluconic acid, accompanied by a sharply decrease in pH to establish a low-pH environment that notably enhanced the catalytic activity of HMMo-zyme, which subsequently drives the conversion of generated H2O2 into toxic hydroxyl radicals (·OH) for amplified anti-bacterial treatment. As a proof of the concept, this NIR-assisted HMMo/GOx@P strategy could efficiently inhibit/kill bacteria and suppress tissue inflammations, thereby accelerating the wound healing processes both in in vitro and in vivo diabetic infection models. This study provides a novel strategy that may serve as a promising alternative for antibiotic therapeutics against diabetic infection, thus holding promise for more effective diabetic infection treatment manipulating Mo-based SAzymes.

Pathogens exploit cellular stress responses to drive infection and evade immune responses, posing a persistent global health threat. Stress granules (SGs), dynamic mRNA hubs formed under stress, and regulated cell death (RCD) pathways collectively orchestrate host-pathogen dynamics. While SGs regulate mRNA translation to aid adaptation, RCD mechanisms-including apoptosis, pyroptosis, and necroptosis-eliminate infected cells to curb pathogen spread. However, pathogens subvert these systems through immune evasion strategies, such as disrupting SGs assembly or hijacking cell death signaling, to enhance replication and persistence. This review integrates molecular insights into SGs biogenesis and RCD regulation, dissecting their bidirectional interplay during infection. We highlight pathogen-specific tactics, such as viral proteases cleaving G3BP1 or bacterial effectors halting translation, to manipulate SGs dynamics and cell death pathways. Furthermore, we explore therapeutic opportunities targeting SGs assembly (e.g., eIF2α phosphorylation modulators, G3BP1 inhibitors) and RCD modulation (e.g., PANoptosis suppression, ferroptosis inducers) to restore host defense and mitigate immunopathology. By bridging molecular mechanisms with clinical applications, this analysis charts a course toward precision therapies leveraging the SGs-RCD axis to combat infectious diseases.

The emergence of drug-resistant strains of Mycobacterium tuberculosis (Mtb), coupled with lengthy treatment cycles and adverse side effects of traditional therapies, poses a significant global challenge in the form of tuberculosis (TB). Photodynamic therapy (PDT) generates reactive oxygen species that target specific tissues or cells via light irradiation at specific wavelengths. It directly disrupts critical structures and components of Mtb to exert its anti-TB effects. Unlike traditional antibiotics that rely on specific targets for efficacy, PDT prevents the occurrence of drug resistance at the mechanism level. Moreover, research indicates that multiple photosensitizers (such as methylene blue and porphyrin derivatives) demonstrate significant bactericidal effects against both drug-sensitive and drug-resistant Mycobacterium tuberculosis in vitro. It can also serve as an adjunct to conventional anti-TB drugs to improve therapeutic efficacy. However, tuberculosis infections predominantly occur in the deep tissues of the lungs. Achieving precise targeted delivery of photosensitizers to the lungs and ensuring their effective activation at deep infection sites, while overcoming the technical limitations of light sources—namely their limited excitation capacity and difficulty in effectively reaching deep pulmonary tuberculosis lesions—has become the core bottleneck for the clinical translation and application of this therapy. In this review, we discuss the principles and mechanisms of PDT, explore the structural characteristics and anti-infective capabilities of various photosensitizers. Finally, we discuss its current clinical applications in tuberculosis patients and future potential, offering novel perspectives for tuberculosis treatment.

Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a major global public health issue, despite improvements in socioeconomic conditions and widespread use of antibiotics. Host immune defense against Mtb infection involve various cells like macrophages, dendritic cells, natural killer cells and T cell subsets, which play distinct roles. By inhibiting phagosome maturation, modulating reactive oxygen and nitrogen species production, regulating host cell death pathway, as well as suppressing antigen presentation and T cell immune responses, the immune escape help Mtb to survive and replicate in macrophages, which ultimately contributes to the development of latent or active TB. While traditional TB treatment strategy suffers challenges like low efficacy, long treatment durations and side effects, the emergence of drug-resistant TB (DR-TB) and multidrug-resistant TB (MDR-TB), which further highlight the therapeutic challenges due to the low cure rate. Host Directed Therapy (HDT) is an emerging supplementary approach to TB treatment, which leverages insights into how host immune cells defend Mtb infection, as well as how pathogens manipulate host immune defense mechanisms. HDT is an approach for treating TB that appropriately modulates host immune responses, which aims to enhance the antimicrobial activity of the host. In this review, we summarized the host immune defense mechanisms, as well as analyzed how Mtb evades host immunological killings, thus potentially providing new insights into the host-pathogen interactions during Mtb infection and TB development. Furthermore, we reviewed recent advances in exploring HDT strategies for effective anti-TB interventions, which may highlight more effective therapeutics to fight against TB.

Tuberculosis (TB), a chronic zoonotic infectious disease caused by Mycobacterium tuberculosis (Mtb) infection, remains a major public health burden worldwide. The increasing threatens of multidrug-resistant/extensively drug-resistant TB, human immunodeficiency virus (HIV) co-infection, lack of effective vaccines and diagnosis methods, as well as the low treatment efficacy of anti-TB therapeutics lead to multiple difficulties and challenges in TB control. Host immune defense is critical for the processes and outcome of Mtb infection control due to the complex immune evasion mechanisms of Mtb, thus, it's of vital importance to characterize the host immune responses and mechanisms during Mtb infection. Nitric oxide (NO) has complex physiological functions in different conditions and has been shown to play important roles in the immune defenses against Mtb infection and even direct killings of Mtb, which still requires further systemic evaluations. In this review, we summarized the current understanding for the roles and mechanisms of NO in host defenses during Mtb infection, as well as the role of NO in the occurrence, development and treatment of TB, which may provide theoretical basis for the development of novel strategies in the prevention and control of TB and drug-resistant TB.