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Human alveolar macrophage metabolism is compromised during Mycobacterium tuberculosis infection

ABSTRACT: Human alveolar macrophage metabolism is compromised during Mycobacterium tuberculosis infection

PROVIDER: PRJNA906986 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22464700.fastq.gz	Fastqsanger.gz
	SRR22464701.fastq.gz	Fastqsanger.gz
	SRR22464702.fastq.gz	Fastqsanger.gz
	SRR22464703.fastq.gz	Fastqsanger.gz
	SRR22464704.fastq.gz	Fastqsanger.gz

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Human alveolar macrophage metabolism is compromised during Mycobacterium tuberculosis infection

Project description:Pulmonary macrophages have two distinct ontogenies: long-lived embryonically-seeded alveolar macrophages (AM) and bone marrow-derived macrophages (BMDM). Here, we show that after infection with a virulent strain of Mycobacterium tuberculosis (H37Rv), primary murine AM exhibit a unique transcriptomic signature characterized by metabolic reprogramming distinct from conventional BMDM. In contrast to BMDM, AM failed to shift from oxidative phosphorylation (OXPHOS) to glycolysis and consequently were unable to control infection with an avirulent strain (H37Ra). Importantly, healthy human AM infected with H37Ra equally demonstrated diminished energetics, recapitulating our observation in the murine model system. However, the results from seahorse showed that the shift towards glycolysis in both AM and BMDM was inhibited by H37Rv. We further demonstrated that pharmacological (e.g. metformin or the iron chelator desferrioxamine) reprogramming of AM towards glycolysis reduced necrosis and enhanced AM capacity to control H37Rv growth. Together, our results indicate that the unique bioenergetics of AM renders these cells a perfect target for Mtb survival and that metabolic reprogramming may be a viable host adjunctive therapy against TB.

2022-12-09 | GSE219072 | GEO

Fc-FcgR interactions shift alveolar macrophage metabolism to promote Mycobacterium tuberculosis restriction in mice

Project description:Fc-FcgR interactions shift alveolar macrophage metabolism to promote Mycobacterium tuberculosis restriction in mice

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Generation of Alveolar Assembloids (AlvAssemb) with Functional Alveolar-like Macrophages

Project description:Within the human lung, interplay between alveolar epithelial cells and resident macrophages shape lung development and function in both health and disease. To study these processes, we devised a strategy for co-culturing hPSC-derived alveolar epithelial organoids and induced macrophages to form functional environment, which we name alveolar assembloids (AlvAssemb). By scRNAseq and functional analysis of AlvAssemb, we identified alveolar type 2-like cells that produced GM-CSF, a response associated with tissue adaptation of macrophages, and that resident alveolar macrophage-like cells secreted interleukin-1β and interleukin-6, a core immune response function, and expressed genes required for surfactant metabolism. Remarkably, in response to alveolar epithelial injury, we found that macrophage-like cells within AlvAssemb efficiently eliminated damaged cells and absorbed oxidized lipids. Moreover, in response to lipopolysaccharide exposure and Mycobacterium tuberculosis infection, we found that core features of the human respiratory defense response were replicated in AlvAssemb. These findings support that AlvAssemb could serve as a valuable platform to investigate human lung development and pathology.

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Human alveolar and splenic macrophage populations display a disctinct transcriptomic response to infection with Mycobacterium tuberculosis

Project description:Mycobacterium tuberculosis (Mtb) infects alveolar macrophages (AMs) causing pulmonary tuberculosis (PTB), the more frequent form of the disease. Less frequently, Mtb disseminates to many other organs and tissues resulting in different extrapulmonary forms of TB. Nevertheless, very few studies have addressed the global mRNA response of human AMs, in particular from humans with the active form of the disease. Strikingly, almost no studies have addressed the response to infection with Mtb by human extrapulmonary macrophages.

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RNA sequencing provides exquisite insight into the manipulation of the alveolar macrophage by tubercle bacilli

Project description:Mycobacterium bovis, the agent of bovine tuberculosis, causes an estimated $3 billion annual losses to global agriculture due, in part, to the limitations of current diagnostics. Development of next-generation diagnostics requires a greater understanding of the interaction between the pathogen and the bovine host. Therefore, to explore the early response of the alveolar macrophage to infection, we report the first application of RNA-sequencing to define, in exquisite detail, the transcriptomes of M. bovis-infected and non-infected alveolar macrophages from ten calves at 2, 6, 24 and 48 hours post-infection. Differentially expressed sense genes were detected at these time points that revealed enrichment of innate immune signalling functions, and transcriptional suppression of host defence mechanisms (e.g., lysosome maturation). We also detected differentially expressed natural antisense transcripts, which may play a role in subverting innate immune mechanisms following infection. Furthermore, we report differential expression of novel bovine genes, some of which have immune-related functions based on orthology with human proteins. This is the first in-depth transcriptomics investigation of the alveolar macrophage response to the early stages of M. bovis infection and reveals complex patterns of gene expression and regulation that underlie the immunomodulatory mechanisms used by M. bovis to evade host defence mechanisms.

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Active Mycobacterium tuberculosis regulatory networks from alveolar macrophages of in vivo mouse infection uncovered by Path-seq

Project description:Transcriptional profiling of Mycobacterium tuberculosis mRNA enriched from host-pathogen samples from in vivo alveolar macrophages (Mus musculus).

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Human alveolar macrophage metabolism is compromised during <i>Mycobacterium tuberculosis</i> infection.

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Project description:The lung environment controls alveolar macrophage metabolism and responsiveness during type-2 inflammation.

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