Tuberculosis Research and Epidemiology

This study shows that senolytic drugs reduce tuberculosis progression in mice by eliminating senescent lung myeloid cells that promote disease.

The paper identifies two distinct cytokine response clusters in healthcare workers resistant to Mtb infection despite exposure, using cytokine profiling and clustering analysis.

The paper evaluates the effectiveness of standard TB drugs in mice, showing rifampin's critical role in killing bacteria and preventing resistance.

This paper uses 3D imaging to show that M. tuberculosis ESX-1 affects granuloma architecture in infected mice.

This study characterizes the structure and interactions of M. tuberculosis Mam1A-1D proteins using X-ray and neutron scattering, revealing their tetrameric structure and disulfide bridges, and their interaction with LucA.

This study integrates transcriptomic, genomic, and GWAS data to identify genes and eQTLs associated with the PB transcriptome response to M. bovis infection in cattle.

This study identifies synergistic combinations of Vancomycin and β-lactams against drug-resistant mycobacteria, showing improved bactericidal activity and reduced bacterial load in vitro and in vivo.

This study shows that targeting CCRL2 with an antibody-drug conjugate improves TB treatment in mice by reducing inflammation and enhancing immune responses.

The paper integrates multi-omic data to identify latent factors associated with resistance to TB conversion, revealing pathways related to multicellular structure and cell-cell interactions.

This study investigates CD4 T cell dysfunction in chronic tuberculosis and links it to bacterial recrudescence in mice.

This paper demonstrates that ATLS2021 enhances sphingolipid levels and improves anti-tubercular efficacy, including sensitizing MDR TB to Rifampicin and inducing immunogenic responses.

This study identifies genetic risk factors for tuberculosis in Brazil using GWAS and single-cell transcriptomics, finding SNPs associated with gene expression in multiple cell types.

This study identifies a master control mechanism for protein secretion in M. tuberculosis involving the ESX-4 system and reveals its role in virulence and host cell interaction.

This study identifies suppressive myeloid cell populations in human TB granulomas using spatial transcriptomics and single-cell immunophenotyping, revealing IDO1+ dendritic cells as key regulators of immune suppression.

This study identifies a candidate transmission survival genome of Mycobacterium tuberculosis by exposing it to model aerosol fluid and analyzing gene contributions to survival during transmission.

The paper identifies Activin A's role in regulating KAT8 and NRF2 to induce ferroptosis during Mycobacterium tuberculosis infection, showing inhibition reduces TB burden.

This study examines how diabetes and tuberculosis co-morbid conditions alter macrophage differentiation and metabolic profiles, revealing perturbed pathways and immune responses.

The paper identifies a TUBB3+ cell population in TB granulomas across multiple species and patients, distinct from known cell types and present in other infections.

This paper evaluates thin-layer agar (TLA) for faster, accurate bedaquiline-susceptibility testing of Mycobacterium tuberculosis directly from sputum samples, achieving high sensitivity and reducing time to result.

This study shows that gluconeogenesis in Mycobacterium tuberculosis is essential for biofilm formation, as it generates glucose for cellulose production in the biofilm matrix.

This study shows that targeting ALOX5/LTA4H signaling reduces TB-induced lung damage and improves bactericidal activity through macrophage-driven inflammation.

The paper identifies a cytokinin-binding protein in M. tuberculosis and shows it binds cytokinins with high specificity, suggesting cytokinins may have roles in mycobacterial physiology.

The paper identifies chemical features affecting mycomembrane permeation and antitubercular activity using a bioorthogonal assay and machine learning.

This study investigates the physiologic recovery of Mycobacterium tuberculosis in mice after antibiotic treatment, finding that recovery is slow, sequential, and incomplete, with longer treatment leading to slower recovery.

The paper uses SEARCH-TB to analyze drug interactions in M. tuberculosis by measuring transcriptional responses to the BPaL regimen in vivo, showing complex effects of drug combinations.

This study identifies in vivo chemical-genetic interactions in tuberculosis that reveal novel drug targets and mechanisms, showing differences from in vitro results and highlighting metabolic dependencies affecting drug efficacy.

The paper shows that most Mtb-specific CD4+ T cells from LTBI individuals recognize infected macrophages, but some require exogenous antigen, and identifies effector functions associated with TB protection.

This study shows that M. tuberculosis uses chalkophores to maintain respiration under copper limitation, which is critical for its virulence in mice.

This study shows that mtDNA mutations in PolgD257A mice increase susceptibility to Mtb by impairing innate immunity and promoting necrosis.

This study reveals how ESAT-6 disrupts the phagosomal membrane through fibril-mediated vesiculation, leading to host cell death and promoting Mtb infection.