---
title: "Gut microbiota and tuberculosis: article content not provided—metadata and access details"
id: "frontiers-in-immunology-14-gut-microbiota-driven-immunomodulation-in-tuberculosis-targeting-dysbiosis-to"
canonical_url: "https://medichelpline.com/clinical-feed/frontiers-in-immunology-14-gut-microbiota-driven-immunomodulation-in-tuberculosis-targeting-dysbiosis-to"
content_type: "clinical_feed_article"
specialty: "Infectious Disease"
source_name: "Frontiers in Immunology"
source_url: "https://www.frontiersin.org/articles/10.3389/fimmu.2026.1889315"
published_at: "2026-08-07T00:00:00.000Z"
evidence_level: "Journal Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Gut microbiota and tuberculosis: article content not provided—metadata and access details
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/frontiers-in-immunology-14-gut-microbiota-driven-immunomodulation-in-tuberculosis-targeting-dysbiosis-to
- **Specialty:** [Infectious Disease](https://medichelpline.com/clinical-feed/infectious-disease.md)
- **Primary Source:** Frontiers in Immunology
- **Source URL:** [Original Journal Publication](https://www.frontiersin.org/articles/10.3389/fimmu.2026.1889315)
- **Published At:** 2026-08-07T00:00:00.000Z
- **Evidence Rating:** Journal Feed
## Executive GIST (TL;DR)
- The provided source content did not include the body of the article titled “Gut microbiota-driven immunomodulation in tuberculosis: targeting dysbiosis to overcome drug resistance.” - Only Frontiers in Immunology website navigation, journal sections, and submission links were present in the source text; no abstract, methods, results, or conclusions were available. - Because the article text and data are absent, specific claims about **gut microbiota**, **dysbiosis**, immunomodulation, or mechanisms linking microbiome changes to **tuberculosis** drug resistance cannot be summarized or paraphrased from this source. - The source confirms the article is hosted on Frontiers in Immunology and that standard journal metadata and section listings were present, but the scientific content was not included. - No study design, experimental details, patient or sample characteristics, outcomes, or recommendations were reported in the provided material. - Readers interested in the full scientific content should access the article directly at the Frontiers site; the source text contained links and site navigation but not the manuscript text itself. - Because facts beyond the site metadata were not available in the source, any clinical or research implications, numerical results, or specific interventions could not be reconstructed or asserted here. - This summary avoids inventing outcomes or recommendations and flags the absence of the full article as the primary limitation of the source material.
## Clinical Analysis & Structured Key Points
Frontiers | Gut microbiota-driven immunomodulation in tuberculosis: targeting dysbiosis to overcome drug resistance REVIEW article Front. Immunol. , 07 August 2026 Sec. Microbial Immunology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1889315 Published in Frontiers in Immunology Microbial Immunology 7 impact factor 11.3 citescore Part of a Research Topic Deciphering host-pathogen interactions in tuberculosis: implications for diagnostics and therapeutics Volume II Submission open 14k views 11 articles Editor & Reviewers Edited by J X Jianping Xie Reviewed by D M Dr. Md. Abdul Alim Al-Bari E J Erfaneh Jafari Outline Figures and Tables Figure 1 View in article Figure 2 View in article Figure 3 View in article Table 1 Clinically validated microbial metabolites in DR-TB pathology. View in article Table 2 Preclinical and clinical evidence for microbiota-targeted interventions in TB management. View in article REVIEW article Front. Immunol. , 07 August 2026 Sec. Microbial Immunology Volume 17 - 2026 | https://doi.org/10.3389/fimmu.2026.1889315 Gut microbiota-driven immunomodulation in tuberculosis: targeting dysbiosis to overcome drug resistance Q N Qi Nie 1,2 † X H Xujuan Hu 1,3 † Y Z Yingjie Zhang 1,3 † L P Ling Pan 1,2 † X Z Xiaoqing Zhang 1,2 Y Z Yong Zhou 1,2 T F Tingting Fu 1,2 L Z Lijuan Zheng 1,2 F X Fan Xiao 1,2 Y L Yuan Liu 1,2 S D Si Du 1,3 J L Jieguang Liu 1,3 L L Leyiyi Liu 1,3 X X Xianglian Xiong 1,3 Y W Yuanjun Wu 1,3 D F Dan Fan 1,3 L T Lixuan Tao 4 * +9 more F R Fuli Ren 1,3,5 * 1. Wuhan Jinyintan Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, China 2. Department of Multidrug-resistant/Drug-resistant Tuberculosis (MDR/DR-TB), Wuhan Jinyintan Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, China 3. Clinical Biospecimen Resource Center, Wuhan Jinyintan Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, Hubei, China 4. Emergency Department, Puren Hospital, Wuhan University of Science and Technology, Wuhan, Hubei, China 5. State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Wuhan, Hubei, China See more Article metrics View details Abstract Tuberculosis (TB) remains a major global health threat, hampered by the escalating prevalence of multidrug-resistant (MDR) and extensively drug-resistant (XDR) strains. Managing these resistant infections demands protracted, intricate, and frequently hepatotoxic drug regimens with poor efficacy, toxicity, and adherence issues. This landscape underscores an urgent need to move beyond a purely antimicrobial-focused paradigm. Converging lines of evidence now firmly position the gut microbiota—a pivotal orchestrator of systemic immunity, metabolic homeostasis, and drug metabolism—as a central determinant in both TB pathogenesis and therapeutic success. Our review describes a vicious cycle at the heart of contemporary TB management. A critical and often overlooked trigger is the profound and persistent gut microbiota dysbiosis induced by the anti-TB medications themselves. Far from an incidental side effect, this dysbiosis is strongly implicated as a pathological driver in preclinical models and observational studies. It undermines pulmonary host defense through the gut-lung axis, aggravates anti-tuberculosis drug-induced liver injury (ATB-DILI), and cultivates a systemic state of chronic inflammation coupled with metabolic dysregulation (such as impaired lipid metabolism). Paradoxically, this host environment fosters Mycobacterium tuberculosis persistence and disease progression. In drug-resistant TB, this vicious cycle is amplified, is associated with therapeutic failure and may contribute to the selection of resistance in correlative studies. To disrupt this cycle, we assess the translational promise of interventions targeting the microbial ecosystem. This encompasses a multi-pronged strategy: employing probiotics, prebiotics, and tailored dietary modifications to restore ecological balance; utilizing fecal microbiota transplantation (FMT) for more profound restoration; and pioneering the development of novel, narrow-spectrum antimicrobials designed to preserve commensal flora. We contend that the integration of microbiome stewardship into TB care is an indispensable evolution in our approach. By concurrently targeting the pathogen and fortifying the host’s intrinsic microbial defenses, this holistic strategy presents a transformative pathway to surmount drug resistance, alleviate treatment-related toxicity, and improve patient outcomes. 1 Introduction Tuberculosis (TB) continues to impose a staggering global health and economic burden, with an estimated 10 million new cases and 1.5 million deaths annually ( 1 ). This persistent crisis is dramatically intensified by the emergence and spread of multidrug-resistant (MDR-TB) and extensively drug-resistant (XDR-TB) strains, which render conventional, prolonged antibiotic regimens increasingly ineffective and toxic ( 2 ). To overcome this impasse, a paradigm shift beyond the traditional pathogen-centric view is urgently needed. The gut microbiota, a vast and dynamic ecosystem of microorganisms, is now recognized as a master regulator of host immunity, metabolism, and drug pharmacology ( 3 ). Dysbiosis, the disruption of this ecosystem, is implicated in a wide array of diseases. In the context of TB, compelling evidence reveals that gut microbiota composition critically influences susceptibility to Mycobacterium tuberculosis ( Mtb ) infection and the efficacy of anti-TB therapy ( 4 ). Crucially, the standard anti-TB drugs themselves induce profound and lasting dysbiosis, creating a detrimental cycle: impaired gut barrier function and altered microbial metabolites compromise systemic immune responses, exacerbate drug-induced hepatotoxicity, and may even foster an environment conducive to the selection of drug-resistant strains ( 5 , 6 ). This recognition of dysbiosis as a central mediator positions gut microbiota disruption not merely as a side effect, but as a central pathological nexus linking treatment failure, adverse outcomes, and drug resistance. This review will first dissect the immunomodulatory mechanisms of the gut-lung axis and the consequences of therapy-induced dysbiosis, before focusing on its specific role in DR-TB. We then critically evaluate microbiota-targeted interventions, and finally, explore the novel frontier of the gut-brain axis in TB patient mental health. This review synthesizes recent advances to systematically delineate the multifaceted role of the gut microbiota in TB pathogenesis and drug resistance. We first dissect the immunomodulatory mechanisms of the gut-lung axis and the consequences of therapy-induced dysbiosis. We then critically evaluate the structural and metabolic alterations of the gut microbiome in DR-TB. Furthermore, we assess the translational potential of microbiota-targeted interventions—including probiotics, FMT, and microbiome-informed drug development—as strategies to restore homeostasis, enhance treatment efficacy, and mitigate adverse effects. Finally, we explore the underappreciated impact of the gut-brain axis on the mental health of TB patients. By integrating perspectives from microbiology, immunology, and clinical medicine, this review aims to chart a path toward innovative, holistic therapeutic strategies that co-manage the pathogen and the host’s microbiome to ultimately overcome the enduring challenge of TB. 2 Gut microbiota and its immune regulatory mechanisms in tuberculosis 2.1 The gut-lung axis: immunomodulatory mechanisms in tuberculosis The gut microbiota is a critical modulator of host immunity, with particular relevance to TB. Through the gut-lung axis, this microbial community exerts remote control over pulmonary immune responses, thereby shaping host defense against Mtb . Gut microbiota composition directly influences the activation and differentiation of CD4+ T cells, a cell population essential for controlling Mtb infection ( 7 ). Gut-derived metabolites, including short-chain fatty acids (SCFAs) and tryptophan derivatives, support immune homeostasis ( 8 ). Among these, the microbial metabolism of tryptophan generates bioactive compounds that activate the aryl hydrocarbon receptor (AhR), a signaling pathway that modulates immune responses and helps sustain immune equilibrium within both the gastrointestinal tract and the systemic compartment ( 9 ). The dynamic interaction between gut microbiota and immune cells encompasses a complex network of signaling pathways. Gut microbiota-derived metabolites enhance the ability of immune cells to detect and respond to pathogens by influencing the expression of pattern recognition receptors (PRRs), which is crucial for initiating appropriate immune responses to Mtb . Furthermore, the gut microbiota influences the adaptive immune response by modulating the differentiation of T helper cells into various subsets, including Th1 and Th17 cells, which are critical for effective anti-tubercular immunity ( 10 , 11 ). Th17 cells—key players in mucosal immunity—are particularly susceptible to gut microbiota influence. Dysbiosis induces an imbalance in Th17 cell activation, thereby contributing to the pathogenesis of TB. The production of interleukin-17 (IL-17) by Th17 cells has been linked to enhanced recruitment of neutrophils and macrophages to the site of infection, facilitating the clearance of Mtb ( 12 ). Dysbiosis, whether induced by malnutrition, comorbidities like obesity, or antibiotic therapy, disrupts this axis, skewing lung immune responses towards a hyperinflammatory state that paradoxically favors Mtb infection and disease progression ( 13 , 14 ). As shown in Figure 1 , anti-TB therapy–induced dysbiosis exemplifies this disruption, creating a vicious cycle that impairs lung immunity, aggravates hepatotoxicity, and promotes drug resistance. Dysbiosis impairs immune responses, characterized by diminished cytokine production and altered T cell populations essential for controlling Mtb infection ( 10 , 11 ). Furthermore, the gut and lung microbiota engage in critical bidirectional communication during Mtb infection. Alterations in the gut microbiome due to antibiotic treatments can lead to dysbiosis, which not only affects gut health but also compromises lung immunity, making the host more susceptible to Mtb colonization ( 15 – 17 ). The presence of certain gut bacteria has also been associated with enhanced expression of protective long non-coding RNAs (lncRNAs) that promote anti-TB immunity ( 18 ). Figure 1 The impact of gut microbiota on immune responses and tuberculosis susceptibility. This diagram illustrates the intricate relationship between gut microbiota, immune responses, and tuberculosis susceptibility. The gut microbiota influences host immunity by modulating CD4+ T cell activity, including the differentiation of Th17 and Tregs. Dysbiosis in the gut microbiota, can impair immune responses, potentially increasing vulnerability to Mtb infection through altered immune system dynamics. In summary, the gut-lung axis is a central regulator of pulmonary anti-mycobacterial immunity. Its dysregulation establishes a permissive environment for Mtb , linking distal intestinal health directly to lung disease outcomes ( 19 , 20 ). Consequently, strategies restoring gut microbiota balance, such as probiotics, FMT, or dietary interventions, represent a promising therapeutic avenue to enhance anti-TB immunity and improve patient outcomes. 2.2 Gut microbiota dysbiosis and susceptibility to tuberculosis A diverse and balanced gut microbiota is a cornerstone of systemic immune competence. In TB, this balance is critically breached. Patients with active disease exhibit a characteristic gut dysbiosis marked by loss of protective commensals and expansion of pro-inflammatory pathobionts. This section details how this specific dysbiotic signature not only reflects disease activity but actively contributes to heightened susceptibility and compromised host defense against Mtb . Research has identified specific alterations in the gut microbiota structure of tuberculosis patients, which may contribute to their heightened susceptibility to the disease. In patients with active TB, there is a marked enrichment of opportunistic pathogens and a depletion of beneficial commensal bacteria. For instance, a comparative study revealed that the gut microbiota of TB patients exhibited a substantial increase in genera such as Escherichia and Shigella , while beneficial taxa like Lactobacillus and Bifidobacterium were significantly reduced ( 21 ). These compositional shifts not only reflect dysbiosis but also suggest a mechanism through which altered gut microbiota impact systemic inflammation and immune responses. It is important to note that the presence of certain pathogenic bacteria may exacerbate inflammatory pathways, leading to a more severe clinical presentation of TB. Furthermore, a dysbiotic gut microbiome is associated with impaired immune function, as evidenced by reduced production of key anti-mycobacterial cytokines ( 22 ). These distinct microbial signatures in TB patients highlight the potential of gut microbiota profiles as biomarkers for susceptibility and as therapeutic targets to restore balance and enhance immunity. However, these associations are subject to significant confounding. Factors such as concurrent antibiotic exposure for other infections, nutritional status—which independently shapes the microbiome—geographic location, which affects both microbiome composition and Mtb strain diversity, and underlying comorbidities including HIV infection or diabetes are rarely fully controlled for in human studies. Therefore, the independent contribution of gut dysbiosis to TB susceptibility remains to be definitively established. 3 The impact of anti-tuberculosis drugs on gut microbiota and its clinical consequences 3.1 Characteristics of gut microbiota dysbiosis induced by anti-tuberculosis drugs The impact of first-line anti-tuberculosis drugs, particularly the combination of isoniazid, rifampicin, pyrazinamide, and ethambutol (HRZE), on gut microbiota diversity and functionality is of critical importance. These medications are imperative in the treatment of TB, but their administration has been associated with substantial alterations in the gut microbiome. HRZE therapy is associated with the utilization of HRZE and a decline in microbial diversity, a hallmark of dysbiosis, which can lead to a decrease in beneficial bacteria, such as those in the genera Bifidobacterium and Lactobacillus , while promoting the growth of potentially harmful bacteria. This dysbiotic shift can, in turn, exacerbate gastrointestinal symptoms and compromise overall health ( 23 ). Moreover, the metabolic functions of the gut microbiota, including the production of SCFAs that play a crucial role in maintaining gut health and immune function, may also be adversely affected. The dysbiotic state induced by HRZE leads to increased intestinal permeability, inflammation, and altered immune responses, which can complicate TB treatment and recovery ( 24 ). Therefore, a comprehensive understanding of these changes is essential for the development of effective strategies to mitigate the adverse effects of anti-TB therapy on gut health. In the context of MDR-TB, the long-term changes in gut microbiota during treatment are of particular concern. The treatment regimens for MDR-TB frequently entail the administration of more potent and toxic medications, which can further disrupt the gut microbiome. Patients undergoing MDR-TB treatment experience sustained dysbiosis, characterized by persistent alterations in gut microbial composition even after the cessation of therapy. This sustained dysbiosis may contribute to complications such as malnutrition and opportunistic infections, which can impair drug pharmacokinetics, delay immune reconstitution, and ultimately hinder treatment success ( 25 ). The long-term implications of such dysbiosis underscore the necessity for meticulous monitoring and potential interventions, such as the administration of probiotics or dietary modifications, to restore gut microbiota balance and support the health of patients undergoing MDR-TB treatment. The intricate relationship between anti-TB therapy and gut dysbiosis warrants further investigation to optimize treatment strategies and enhance patient outcomes. The degree and duration of dysbiosis vary considerably, depending on factors such as the specific drug regimen—whether first-line or MDR-TB therapy—treatment duration, and host genetics. Moreover, the clinical relevance of particular taxonomic shifts, including decreases in Lactobacillus or Bifidobacterium , is frequently extrapolated from other disease contexts and may not be directly applicable to tuberculosis. The absence of standardized protocols for microbiome sampling and analysis across studies further limits comparability. 3.2 Gut microbiota dysbiosis and antituberculosis drug-induced liver injury The hepatotoxicity of anti-TB drugs is a major clinical setback, and the gut-liver axis serves as a crucial mediator of this adverse effect. Drug-induced gut dysbiosis compromises intestinal barrier integrity, facilitating the translocation of microbial products that ignite hepatic inflammation and oxidative stress. Here, we dissect this cascade and highlight the emerging role of gut microbiota modulation as a strategic avenue to mitigate ATB-DILI. Probiotics, particularly strains such as B. fragilis 839 , have emerged as promising therapeutic agents in the context of drug-induced liver injury, particularly in patients undergoing antituberculosis therapy. The mechanisms by which B. fragilis 839 exerts its hepatoprotective effects are multifactorial. One of the primary mechanisms involves the restoration of gut microbiota diversity, which is often compromised during antituberculosis treatment. By re-establishing a balanced microbial community, probiotics can enhance the integrity of the intestinal barrier, thereby reducing intestinal permeability and preventing the translocation of harmful substances, such as endotoxins, into the bloodstream. Reducing systemic inflammation is crucial, as elevated levels of inflammatory cytokines contribute to the pathogenesis of drug-induced liver injury. Furthermore, B. fragilis 839 has been observed to produce metabolites, such as SCFAs, which have been shown to possess anti-inflammatory properties and can promote liver health by modulating immune responses and reducing oxidative stress. A series of experimental studies have demonstrated that the administration of B. fragilis 839 can significantly lower serum levels of liver enzymes, including alanine aminotransferase (ALT) and aspartate aminotransferase (AST). These enzymes are often used as indicators of liver injury. Furthermore, histopathological examinations revealed improvements in liver architecture, with reduced signs of inflammation and necrosis in treated animals. These findings demonstrate the value of probiotics not only as adjunctive therapies to alleviate ATB-DILI but also as preventive measures to enhance the overall safety and efficacy of anti-TB treatments ( 13 ). Future clinical trials are needed to further elucidate the specific pathways involved and establish standardized probiotic interventions in clinical practice. 3.3 The impact of gut microbiota dysbiosis on treatment outcomes and drug resistance The gut microbiota plays a crucial role in the efficacy of various pharmacological treatments, particularly in the context of TB and its drug-resistant forms. In a murine model, antibiotic-induced dysbiosis was shown to reduce the efficacy of isoniazid (INH), a first-line anti-TB medication, by compromising host immune responses and impairing the clearanc
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