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The BCG Delta BCG1419c vaccine candidate reduces lung pathology, IL-6, TNFa, and IL-10 during chronic TB infection

ABSTRACT: The BCG Delta BCG1419c vaccine candidate reduces lung pathology, IL-6, TNFa, and IL-10 during chronic TB infection

PROVIDER: PRJNA454371 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7086711_1.fastq.gz	Fastqsanger.gz
	SRR7086711_2.fastq.gz	Fastqsanger.gz
	SRR7086712_1.fastq.gz	Fastqsanger.gz
	SRR7086712_2.fastq.gz	Fastqsanger.gz
	SRR7086713_1.fastq.gz	Fastqsanger.gz

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The BCG Delta BCG1419c vaccine candidate reduces lung pathology, IL-6, TNFa, and IL-10 during chronic TB infection

Project description:Comparison of transcriptional differences (RNA-seq) between BCG delta1419c and wild-type BCG that might explain the pathological differences in vaccination studies.

2018-06-20 | GSE113888 | GEO

The BCG?BCG1419c Vaccine Candidate Reduces Lung Pathology, IL-6, TNF-?, and IL-10 During Chronic TB Infection.

Project description:Mycobacterium tuberculosis (M. tuberculosis), the causative agent of human tuberculosis (TB), is estimated to be harbored by up to 2 billion people in a latent TB infection (LTBI) state. The only TB vaccine approved for use in humans, BCG, does not confer protection against establishment of or reactivation from LTBI, so new vaccine candidates are needed to specifically address this need. Following the hypothesis that mycobacterial biofilms resemble aspects of LTBI, we modified BCG by deleting the BCG1419c gene to create the BCG?BCG1419c vaccine strain. In this study, we compared cytokine profiles, bacterial burden, and lung lesions after immunization with BCG or BCG?BCG1419c before and after 6 months of aerosol infection with M. tuberculosis H37Rv in the resistant C57BL/6 mouse model. Our results show that in infected mice, BCG?BCG1419c significantly reduced lung lesions and IL-6 in comparison to the unmodified BCG strain, and was the only vaccine that decreased production of TNF-? and IL-10 compared to non-vaccinated mice, while vaccination with BCG or BCG?BCG1419c significantly reduced IFN-? production. Moreover, transcriptome profiling of BCG?BCG1419c suggests that compared to BCG, it has decreased expression of genes involved in mycolic acids (MAs) metabolism, and antigenic chaperones, which might be involved in reduced pathology compared to BCG-vaccinated mice.

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Deletion of nuoG in recombinant BCG vaccine against TB

Project description:The current tuberculosis vaccine, Bacillus Calmette-Guérin (BCG), provides insufficient protection. We deleted the NADH dehydrogenase 1 subunit G (nuoG) gene from BCG ΔureC::hly, the most advanced live vaccine candidate in clinical development. Removal of nuoG enhanced co-localisation of LC3 to bacteria in human host cells. BCG ΔureC::hly ΔnuoG vaccination was safer than BCG and improved efficacy of BCG ΔureC::hly by reducing tuberculosis load in murine lungs 1000-fold.

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Project description:Treatment with IL-1b or TNFa enhance the proliferation of alveolar type 2 cells in organoid culture. Here, we examine the downstream mechanisms that enhance AEC2 proliferation after IL-1b and TNFa treatments, we performed RNA-seq analysis of AEC2s isolated from organoids 6 hrs after exposure to either cytokine. We identified 165 differentially expressed genes that were common in both IL-1b and TNFa treated AEC2s compared to saline treated controls.

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Project description:Proper inflammatory responses are vital to restore tissue homeostasis against offending factors. However, it is largely under explored whether inflammatory responses are modulated by the Hippo effectors YAP/TAZ. To identify the transcription targets related to inflammatory reponses for YAP, we utilized human bronchioalveolar carcinoma cells H358 expressing YAP(5SA) or GFP (as a control) and treated with vehicle, TNFa or IL-1b, respectively. Our work disclosed the complex features of YAP/TAZ’s role in inflammatory responses.

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Discovery of YAP target genes with TNFa or IL-1b induction

Project description:Discovery of YAP target genes with TNFa or IL-1b induction

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Tissue-resident macrophages promote multiple myeloma early dissemination and progression via IL-6 and TNFa

Project description:Multiple myeloma (MM) is a plasma cell malignancy characterized by the presence of multiple foci in the skeleton. These distinct tumor foci indicate cycles of tumor growth and dissemination that seed new clusters and drives disease progression. Utilizing an intra-tibial Vk*MYC murine myeloma, we found that CD169 + radiation-resistant, tissue-resident macrophages (MPs) were critical for myeloma early dissemination and disease progression. While depletion of these MPs had no effect on tumor proliferation, it reduced myeloma BM egress and spreading to other bones, which improved overall survival as a single therapy and in combination with BM transplantation. Myeloma dissemination correlated with an increased inflammatory signature in BM MPs, as well as production of IL-6 and TNFα by tumor-associated MPs (TAMs). Exogenous i.v. IL-6 and TNFa could trigger myeloma intravasation in the BM by increasing vascular leakiness in the BM, and by enhancing myeloma motility by reducing CD138 adhesion. Moreover, mice lacking IL-6 had defects in myeloma dissemination as in MP-depleted recipients. While in TNFa or TNFaR deficient mice had defects in MM dissemination, engraftment was also impaired. These effects on myeloma dissemination required production of cytokines in the radiation-resistant compartment, containing these radiation-resistant BM MPs. Taken together, we propose BM egress of myeloma cells is regulated by localized inflammation in foci, driven in part by CD169 + MPs.

2021-06-09 | GSE176385 | GEO

Nonpathogenic SIV and Pathogenic HIV Infections Associate with Disparate Innate Cytokine Signatures in Response to M. bovis BCG

Project description:Infections with mycobacteria, including Mycobacterium tuberculosis (Mtb) and Mycobacterium bovis (M. bovis) BCG, are a leading cause of morbidity and mortality for HIV-infected persons. In contrast to HIV, SIV infection of sooty mangabeys is nonpathogenic, characterized by a lack of clinical disease including an absence of opportunistic infections. The goal of this study was to identify innate immune responses to M. bovis BCG maintained during nonpathogenic lentiviral infections, through a comparison of functional responses during pathogenic HIV or nonpathogenic SIV infections. Monocytes were evaluated for their ability to express key anti-mycobacterial cytokines TNF-α and IL-12 following a six-hour ex vivo BCG exposure. While HIV-infection was associated with a decreased percentage of IL-12-producing monocytes, nonpathogenic SIV-infection was associated with an increased percentage of monocytes producing both cytokines. Gene expression analysis of PBMC following ex vivo BCG exposure identified differential expression of NK cell-related genes and several cytokines, including IFN-γ and IL-23, between HIV-infected and control subjects. In contrast, SIV-infected and uninfected-control mangabeys exhibited no significant differences in gene expression after BCG exposure. Finally, differential gene expression patterns were identified between species, with mangabeys exhibiting lower IL-6 and higher IL-17 in response to BCG when compared to humans. Overall, this comparison of immune responses to M. bovis BCG identified unique immune signatures (involving cytokines IL-12, TNF-α, IL-23, IL-17, and IL-6) that are altered during HIV, but maintained or increased during nonpathogenic SIV infections. These unique cytokine and transcriptome signatures provide insight into the differential immune responses to Mycobacteria during pathogenic HIV-infection of humans or nonpathogenic SIV-infection of mangabeys.

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