Tuberculosis结核病
Tuberculosis(英文缩写 TUBERCULOSIS),ISSN 1472-9792,eISSN 1873-281X,中文译名:结核病 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.973 | Q3 |
| 2022 | 3.200 | Q3 |
| 2023 | 2.800 | Q2 |
| 2024 | 2.900 | Q2 |
| 2025 | 2.900 | Q2 |
Tuberculosis 最新收录文献
-
1. Exploratory proteomic and metabolomic profiling of pleural effusions identifies histone H4 and alanine as promising complementary markers for pleural tuberculosis.
PMID:日期:2026-08-17The diagnosis of pleural tuberculosis (Pl-TB) remains challenging. Histopathological analysis and pathogen detection in pleural biopsies are informative but limited. We investigated differentially expressed proteins and metabolites in pleural effusions from patients with Pl-TB, malignancies, and other pathologies. A proteomic analysis of pooled pleural effusions identified 45 proteins exclusively detected or upregulated in Pl-TB samples, many linked to infectious processes. Conversely, 18 proteins were uniquely found or upregulated in malignant pleural effusions, mainly associated with detoxification and hemostasis. To validate these findings, we employed targeted proteomics in individual samples. Eight proteins were validated: S100-A9, histone H4, insulin-like growth factor-binding protein 2, fibrinogen beta chain, ficolin-3, immunoglobulin heavy constant alpha 1, sulfhydryl oxidase 1, and histidine-rich glycoprotein. Additionally, NMR-based metabolomics identified 13 metabolites with differential abundance between Pl-TB and non-TB samples. Notably, N-acetyl-glycoprotein and the branched-chain amino acids, alanine and lysine differed between groups. Proteomic and metabolomic analyses revealed distinct molecular profiles between Pl-TB and non-TB patients, despite intra-group variability. To address this, we applied classification models. Histone H4 and alanine consistently emerged as discriminative features. Overall, this study provides novel insights into the molecular landscape of Pl-TB. The combined quantification of proteins and metabolites may improve differential diagnosis, although should be further validated in larger, independent cohorts before clinical application.
-
3. Glycaemic burden disrupts innate immunity in TB by modulating CD206 expression and macrophage antimicrobial responses.
PMID:日期:2026-08-04Tuberculosis (TB) and diabetes mellitus (DM) represent a growing dual global health burden, with chronic hyperglycaemia recognized as a major modifier of host immunity against Mycobacterium tuberculosis (Mtb). Macrophages, central to pathogen recognition, phagocytosis, antigen presentation, and intracellular killing, may be particularly vulnerable to diabetic metabolic dysregulation. This study evaluated phenotypic and functional macrophage alterations in individuals with pulmonary TB, type 2 DM, TB-DM comorbidity, and healthy controls. Surface receptor expression was analysed by multicolour flow cytometry, while phagocytosis and intracellular bacterial clearance were assessed using FITC-labelled Mtb assays and colony-forming unit enumeration. Hyperglycaemia was associated with reduced CD11b, MARCO, and TLR2 expression alongside upregulation of the mannose receptor CD206, which correlated positively with HbA1c levels, indicating a shift toward a permissive M2-like phenotype. Phagocytic uptake of Mtb was significantly impaired and inversely correlated with HbA1c. Antigen-presenting capacity was selectively compromised, with reduced CD80 and CD86 expression in DM and TB-DM groups, while HLA-DR remained unchanged. Intracellular Mtb killing was markedly diminished in diabetic macrophages. These findings demonstrate that chronic hyperglycaemia profoundly disrupts macrophage innate immunity, contributing to increased TB susceptibility and poor infection control in diabetic populations.
-
4. Drug resistance in tuberculous meningitis: A laboratory-based observational study from Northern India's tertiary care referral centre.
PMID:日期:2026-07-20Tuberculous meningitis (TBM) is the most severe form of tuberculosis and is associated with high mortality and long-term neurological disability. Detection of drug resistance remains challenging because cerebrospinal fluid (CSF) specimens are typically paucibacillary and often available only in limited volumes. This retrospective laboratory based study characterized drug-resistance patterns and diagnostic attrition across the laboratory testing cascade using CSF samples from patients with presumed TBM referred between January 2023 and December 2025 in a high tuberculosis-burden setting. Samples underwent Mycobacterium tuberculosis cartridge-based nucleic acid amplification testing (CBNAAT), automated liquid culture, line probe assays and phenotypic drug susceptibility testing according to national guidelines. Of 8926 CSF samples tested by CBNAAT, 812 (9.0%) were positive for M. tuberculosis. Rifampicin resistance was detected in 17.0% (138/812; 95% CI: 14.6-19.7) of positive cases. Only 837 samples had sufficient volume for culture, of which 58 (6.9%; 95% CI: 5.4-8.9) were culture-positive. Among these isolates, 29 (50.0%; 95% CI: 37.5-62.5) were multidrug resistant (MDR-TB). Six MDR isolates were also fluoroquinolone resistant, including one extensively drug-resistant (XDR-TB) isolate. These findings demonstrate a high burden of drug resistance, substantial diagnostic attrition, and the need to expand access to comprehensive drug-susceptibility testing in TBM.
-
5. FadR subfamily of transcriptional regulators are dispensable for the pathogenesis of Mycobacterium tuberculosis.
PMID:日期:2026-07-11A diverse set of transcriptional regulators (TRs) enables Mycobacterium tuberculosis (M. tuberculosis) to reprogram its gene expression profiles to adapt and counteract the challenges imposed by the host during infection. FadR subfamily TRs regulate different physiological aspects of bacteria, including stress adaptation and virulence. The genome of M. tuberculosis encodes five homologs of the FadR subfamily of TRs. Here, we have comprehensively characterised the three FadR subfamily TRs, namely Rv0043c, Rv0165c, and Rv3060c, to assess their role in M. tuberculosis stress adaptation and pathogenesis. We demonstrate that the individual deletion of these TRs does not affect the growth of M. tuberculosis in vitro under various host-mimicking stress conditions or during infection of macrophages, mice, or guinea pigs. RNA-seq analysis revealed that, compared to the wild type strain, the relative transcript levels of the majority of differentially expressed genes were increased in the ΔRv0043c, ΔRv0165c and ΔRv3060c strains of M. tuberculosis, suggesting that these proteins function as transcriptional repressors. Taken together, these results suggest that functional redundancy exists between the FadR subfamily of TRs.
-
6. Multiparametric flow cytometry immune profiling of pulmonary and extra-pulmonary tuberculosis reveals distinct blood-based biomarker signatures.
PMID:日期:2026-07-09This study investigated immune cell distributions, cell-specific immune markers, and selected biomarker targets in pulmonary tuberculosis (PTB) and extrapulmonary tuberculosis (EPTB) using multiparametric flow cytometry (MFC). Whole blood was collected from 45 individuals, including healthy controls (HC), EPTB, and PTB patients (n = 15/group). Peripheral blood leukocytes were analysed by MFC to characterize CD4 and CD8 T cells, natural killer (NK), invariant NKT (iNKT) and NKT cells, classical (CM), intermediate (IM) and non-classical monocytes (NCM), and activated monocytes (AM). Expression of GBP1, CALCOCO2, IFIT3, SNX10, ARG1, PD-1, and PD-L1 was assessed across these immune subsets. Increased frequencies of NK, NKT, and monocytes were observed in PTB and EPTB compared with HC, while CD4, CD8, iNKT, and AM were reduced. Monocyte-to-lymphocyte ratios were incrementally elevated in EPTB and PTB compared with HC. Despite variability of expression within groups, median biomarker fold-change expression changes were found between HC, EPTB and PTB groups; (i) (>2.0FC) for ARG1 in CD4, CD8, CM and AM, for CALCOCO2 in AM, GBP1 in CD8 and NCM, PD-1 in CD4, CD8, NK, IM and AM, PD-L1 in CD4, CD8, iNKT and NKT, NK, IM and AM and SNX10 in CD4, CD8, NCM, IM and AM (ii) (<2.0FC) in TB vs HC for CALCOCO2 in iNKT and NKT, IFIT3 in NCM, PD-1 in NK and NCM, PD-L1 in NCM, IM and AM and SNX10 in AM. Statistical significance was achieved for ARG1 (P = 0.017) in CD4 cells. Our findings highlight distinct immune cell and biomarker signatures in PTB and EPTB.
-
7. Host-derived proteomic biomarkers for discriminating the tuberculosis disease spectrum in a Brazilian cohort.
PMID:日期:2026-06-26Despite significant efforts to improve diagnostics, tuberculosis (TB) diagnosis still relies on clinical and laboratory methods limited by cost, expertise, and time. Early diagnosis is essential for effective management of pulmonary TB (PTB), pleural TB (PLTB), and latent TB infection (LTBI), highlighting the urgent need for rapid, accurate, and accessible TB diagnostics based on low-invasive sampling. In this study, a quantitative rapid test, previously evaluated in European and African cohorts, was applied to a Brazilian cohort to measure six host-derived proteins in serum from individuals with PTB, PLTB, other pleural diseases (OPLD), LTBI, and controls. Serum levels of CRP, ferritin, and SAA1/A2 were significantly elevated in PTB and PLTB compared to controls. SAA1/A2 and IP-10 levels were higher in PLTB compared to LTBI. Furthermore, IP-10 serum levels showed diagnostic potential, as they were elevated in PTB compared with both LTBI and controls, and significantly increased in PLTB compared to OPLD. In pleural effusion, IP-10, IL-6, and S100A12 were significantly higher in PLTB than in OPLD, while ferritin levels were higher in OPLD. Our study shows that quantitative detection of host-derived biomarkers identified for active PTB in European and African populations can support clinical decision-making for TB spectrum in a Brazilian setting.
-
8. Association between gut microbiota and white matter microstructural damage in tuberculous meningitis patients.
PMID:日期:2026-06-17Tuberculous meningitis (TBM), the most severe form of tuberculosis, may involve the gut-brain axis. This study investigated the link between TBM, brain white matter integrity measured by diffusion tensor imaging (DTI), and the gut microbiome. 22 TBM patients and 31 healthy controls underwent MRI and provided fecal samples. Gut microbiota (16S rRNA sequencing), fecal metabolites (metabolomics), and DTI metrics (FA, MD, RD, AD) were analyzed. Tract-based spatial statistics and correlation analyses were employed. TBM patients showed lower gut microbiota α-diversity. The abundance of the Escherichia genus correlated negatively with FA and positively with MD in specific white matter tracts. Metabolomics revealed elevated acetic acid in TBM patients, which correlated with both Escherichia abundance and DTI metrics. KEGG analysis indicated altered arginine and proline metabolism pathways. TBM is associated with differences in gut microbiota composition. Higher relative abundance of Escherichia is linked to white matter microstructural damage, potentially mediated by specific bacterial metabolites.
-
9. Context-dependent transcriptional and epigenetic reprogramming shapes neutrophil antimicrobial and immunoregulatory functions in tuberculosis.
PMID:日期:2026-06-13Inflammatory microenvironments regulate immune cell differentiation, activation, and programming. Although traditionally considered terminally differentiated effectors, neutrophils can acquire distinct functional states in response to environmental cues. To examine context-dependent neutrophil programming, cells from healthy donors were cultured in vitro under cytokine regimens mimicking opposing inflammatory environments (GM-CSF/IFN-γ or IL-4/IL-13/TGF-β), alone or combined with PMA and Mycobacterium tuberculosis, to assess functional and transcriptional responses. GM-CSF/IFN-γ-conditioned neutrophils exhibited increased cell size, altered nuclear morphology, enhanced MHC class II and CD86 expression, and elevated IL-8 and reactive oxygen species production. This profile was associated with increased TNF-α, IL-10, TLR2, and TLR4 gene expression and reduced global DNA methylation. In contrast, IL-4/IL-13/TGF-β-conditioned neutrophils resembled non-conditioned controls regarding surface markers and cytokine production but showed reduced ROS generation and increased DNMT3A expression. Upon in vitro infection with M. tuberculosis, GM-CSF/IFN-γ-conditioned neutrophils produced higher IL-8 and IL-1β levels and formed more neutrophil extracellular traps. Additionally, plasma from patients with severe tuberculosis modulated TLR4, CCR7, and IP-10 expression in healthy neutrophils, indicating systemic inflammatory influences. These findings demonstrate that inflammatory conditioning induces coordinated transcriptional and epigenetic remodeling, shaping neutrophil antimicrobial and immunoregulatory potential in infectious contexts.
-
10. Association of vitamin D status with the immune response in active pulmonary tuberculosis patients with chronic pulmonary aspergillosis.
PMID:日期:2026-05-22The aim of the study was to determine the associations between vitamin D (VD) and cytokine levels in active pulmonary tuberculosis (PTB) patients with chronic pulmonary aspergillosis (CPA). One hundred seventy-two active PTB patients, twenty-eight PTB patients with CPA (PTB-CPA), and sixty healthy subjects were included in the study. The concentrations of serum 25-hydroxyvitamin D, interleukin (IL)-1β, IL-4, IL-6, IL-8, IL-10 and tumor necrosis factor (TNF-α) were measured by ELISA. A significantly lower VD level was detected in PTB-CPA patients (14.96 ± 10.89 ng/mL) than in both PTB patients (20.72 ± 8.07 ng/mL, p < 0.01) and controls (23.90 ± 8.16 ng/mL, p < 0.001). VD deficiency was significantly more prevalent in PTB-CPA patients than in PTB patients (OR = 2.86, 95% CI: 1.22-6.69; p = 0.01) or controls (OR = 5.33, 95% CI: 2.02-14.11; p = 0.0005). In the PTB group, VD levels exhibited a significant inverse correlation with only IL-6 (r = -0.376, p = 0.0001), whereas in PTB-CPA patients, stronger inverse correlations were observed with IL-6 (r = -0.691, p = 0.0005) and IL-8 (r = -0.538, p = 0.01). In cavitary PTB patients, a significant inverse link was found between VD and IL-1β and IL-6 levels (all p ≤ 0.05). Our data revealed a high prevalence of VD deficiency in all groups, predominantly in PTB-CPA patients. The inverse correlations between VD levels and IL-6 and IL-8 levels in PTB-CPA patients as well as between VD and IL-1β and IL-6 levels in cavitary PTB patients, provide further evidence for the role of VD as a regulator of inflammatory pathways in the context of coinfection.