ArticleMolecular therapy : the journal of the American Society of Gene Therapy2024
Intranasal vaccination with engineered BCG expressing CCL2 induces a stronger immune barrier against Mycobacterium tuberculosis than BCG.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- ESAT-6-derived lipopeptide-based mucosal vaccine elicits distinct humoral immune responses concomitant with a reduction inEmerging microbes & infections · 2026Article
- Mucosal BCG Vaccination and Immune Layering: Route-Dependent Programming of Immunity at the Respiratory Interface.Vaccines · 2026Review
- Emerging insights into CC and CXC chemokines and their receptors in Mycobacterium tuberculosis infection.FEBS open bio · 2026Review
- Antimicrobial therapy combined with C-C chemokine receptor type 2 modulation dampens mycobacteria-aggravated monocyte activation and atherosclerosis.Frontiers in cardiovascular medicine · 2026Article
- Leveraging a synthetic biology approach to enhance BCG-mediated expansion of Vγ9Vδ2 T cells.PloS one · 2026Article
- Intranasal vaccines adjuvanted with Nexavant demonstrate robust protective efficacy by inducing both mucosal and systemic immunity in a murine model.Frontiers in immunology · 2025Article
- Does increased CCL2-mediated immune cell recruitment during mucosal BCG vaccination provide superior protection against TB?Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intradermal Mycobacterium bovis Bacillus Calmette-Guérin (BCG) vaccination is currently the only licensed strategy for preventing tuberculosis (TB). It provides limited protection against pulmonary TB. To enhance the efficacy of BCG, we developed a recombinant BCG expressing exogenous monocyte chemoattractant CC chemokine ligand 2 (CCL2) called rBCG-CCL2. Co-culturing macrophages with rBCG-CCL2 enhances their abilities in migration, phagocytosis, and effector molecule expression. In the mouse model, intranasal vaccination with rBCG-CCL2 induced greater immune cell infiltration and a more extensive innate immune response in lung compared to vaccination with parental BCG, as determined by multiparameter flow cytometry, transcriptomic analysis, and pathological assessments. Moreover, rBCG-CCL2 induced a high frequency of activated macrophages and antigen-specific T helper 1 (Th1) and Th17 T cells in lungs. The enhanced immune microenvironment responded more effectively to intravenous challenge with Mycobacterium tuberculosis (Mtb) H37Ra, leading to significant reductions in H37Ra burden and pathological damage to the lungs and spleen. Intranasal rBCG-CCL2-vaccinated mice rapidly initiated pro-inflammatory Th1 cytokine release and reduced pathological damage to the lungs and spleen during the early stage of H37Ra challenge. The finding that co-expression of CCL2 synergistically enhances the immune barrier induced by BCG provides a model for defining immune correlates and mechanisms of vaccine-elicited protection against TB.
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