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Mycobacterial DNA binding protein 1 (MDP1) mediates gene regulation in Mycobacterium tuberculosis variant Bacillus Calmette-Guerin

ABSTRACT: Mycobacterial DNA binding protein 1 (MDP1) mediates gene regulation in Mycobacterium tuberculosis variant Bacillus Calmette-Guerin

PROVIDER: PRJNA918672 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22989358_1.fastq.gz	Fastqsanger.gz
	SRR22989358_2.fastq.gz	Fastqsanger.gz
	SRR22989359_1.fastq.gz	Fastqsanger.gz
	SRR22989359_2.fastq.gz	Fastqsanger.gz
	SRR22989360_1.fastq.gz	Fastqsanger.gz

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Mycobacterial DNA binding protein 1 (MDP1) mediates gene regulation in Mycobacterium tuberculosis variant Bacillus Calmette-Guerin

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Project description:Bacille Calmette Guerin (BCG) is the most widely administered vaccine in the world yet its mechanism of action remains unclear. In this study, we have used samples from a human mycobacterial challenge study in which previously BCG-vaccinated or BCG-naïve UK adults were challenged intradermally with a standard dose of BCG vaccine. BCG remaining at the site of vaccination was quantified by polymerase chain reaction from a skin biopsy sample taken two weeks post-challenge and was used as a measure of BCG growth and functional anti-mycobacterial immunity. Using gene expression microarrays and flow cytometric analysis of intracellular cytokine production, we show that the magnitude of the immune response is greater in previously vaccinated volunteers and that this correlates with reduced mycobacterial growth but increased scarring at the vaccination site. In particular the IFNγ and IL-17 pathways are strongly induced in previously vaccinated volunteers and correlate with reduced mycobacterial growth in this population. This study supports the use of BCG challenge as a tool for evaluating vaccine efficacy and identifying mechanisms of anti-mycobacterial immunity

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Project description:Intralesional therapy using Mycobacterium bovis Bacillus Calmette-Guérin (BCG) for cutaneous metastatic melanoma induces regression of injected, but also non-injected lesions. Tumor-associated macrophages (also known as M2) infiltrate solid tumors and impair antitumor immunity. Since macrophages play a pivotal role in both tumors and mycobacterial infections, we hypothesized BCG alters M2 to promote antitumor immunity. BCG-treated, in vitro-polarized M2 (M2-BCG) show dramatic transcriptional changes involving inflammation, immune cell recruitment, cross-talk and activation pathways. Mechanistic network analysis indicates potential for M2-BCG to improve IFN-γ responses, frequently used as a marker for successful antitumor immunity. Accordingly, we found an increased frequency of IFN-γ-producing CD4+ T cells responding to M2-BCG vs mock-treated M2 (p<0.05). Moreover, supernatant from M2-BCG increased the frequency of granzyme B-producing CD8+ tumor-infiltrating lymphocytes (TIL) responding to autologous melanoma cell lines (p<0.01). Comparing the transcriptome of injected vs uninjected lesions biopsied from IL-BCG patients showed immune function prevailing in injected lesions, with the most enriched pathways representing T cell activation mechanisms. In vitro BCG-infected tumor cells also stimulated IFN-γ production from HLA-A2-restricted syngeneic TIL from the same melanoma patient (p<0.05). Together, our data indicates BCG can promote an antitumor microenvironment in cutaneous metastatic melanoma.

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Project description: Not available

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