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ABSTRACT: Mycobacterium tuberculosis infection progression in cynomolgus macaques

PROVIDER: PRJNA1236326 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32700200_1.fastq.gz	Fastqsanger.gz
	SRR32700201_1.fastq.gz	Fastqsanger.gz
	SRR32700202_1.fastq.gz	Fastqsanger.gz
	SRR32700203_1.fastq.gz	Fastqsanger.gz
	SRR32700204_1.fastq.gz	Fastqsanger.gz

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Project description:Human infection with Mycobacterium tuberculosis results in a continuum of ill-defined, clinical manifestations with stable latent M. tuberculosis infection (LTBI) and severe active disease at the ends. Identifying different states of infection is of importance to tuberculosis (TB) control since risk of developing active disease varies among different asymptomatic states while infectiousness varies among patients with different bacterial burden. We investigated changes in proteome-scale antibody responses during disease progression in a non-human primate model of tuberculosis. We probed M. tuberculosis proteome microarrays with serial sera collected from three infection-outcome groups (active, reactivation, and latent). We found that each infection outcome is associated with characteristic changes in the antibody levels and number of antigenic targets, which suggested an association between antibody responses and bacillary burden. Additional proteome-scale serological profiling of > 400 human TB suspects established that antibody responses are positively associated with bacterial load. Thus tuberculosis-specific antibody levels and number of antigenic targets increases with disease progression. To investigate antibody responses during the course of infection, we probed M. tuberculosis proteome microarrays with serial sera collected from experimentally infected cynomolgus macaques. Based on infection outcome, the macaques were grouped into three classes; A) active disease (n = 4), B) latent infection (n=5) and C) reactivation disease (n = 5). Note that the macaques in the reactivation class developed signs of disease spontaneously without any experimental intervention. For each animal, we tested one pre-infection time point and approximately ten post-infection time points at one-month intervals.

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Project description:This longitudinal dataset was generated to assess changes in whole blood gene expression following low dose Mycobacterium tuberculosis infection of Cynomolgus macaques. In addition to changes in mRNA transcript abundance, changes in circulating immune cell populations were also assessed using both complete blood counts (CBC) and using flow cytometry. Disease severity was determined using both clinical diagnosis (active vs. latent) and 18F-flurodeoxyglucose (FDG avidity) by 6 months post-infection. The greatest change in transcriptional activity occurred 20-56 days after infection, when the maximum activity of immune related transcripts was observed. After stratifying macaques based on clinical diagnosis, those macaques with active disease exhibited a similar signature to that observed in humans with active TB. However, only modest transcriptional differences between active TB and latently infected macaques were observed. As an alternative stratification approach, the severity of lung inflammation measured by lung FDG avidity was used to separate macaques into high and low FDG groups. Blood transcript activity was highly correlated with lung inflammation at early time points post-infection. The differential expression signatures between animals stratified with high and low lung FDG were stronger than those observed with groups defined by clinical outcome.. Furthermore, gene level analysis of of pre-infection signatures suggest that interferon and inflammation signatures may distinguish eventual clinical outcomes and lung FDG avidity prior infection. In conclusion, this study demonstrates that transcriptional changes in the macaque model recapitulate those observed in human Mtb infection while providing additional insight into the early and pre-infection events associated with disease severity and outcome.

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