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Serum Amyloid A proteins reduce bone mass during mycobacterial infections

ABSTRACT: Serum Amyloid A proteins reduce bone mass during mycobacterial infections

PROVIDER: PRJNA891037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21922514.fastq.gz	Fastqsanger.gz
	SRR21922515.fastq.gz	Fastqsanger.gz
	SRR21922516.fastq.gz	Fastqsanger.gz
	SRR21922517.fastq.gz	Fastqsanger.gz
	SRR21922518.fastq.gz	Fastqsanger.gz

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Serum Amyloid A proteins reduce bone mass during mycobacterial infections

Project description:To investigate the molecular mechanisms responsible for bone loss during mycobacterial infections

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Serum amyloid A proteins reduce bone mass during mycobacterial infections.

Project description:IntroductionOsteopenia has been associated to several inflammatory conditions, including mycobacterial infections. How mycobacteria cause bone loss remains elusive, but direct bone infection may not be required.MethodsGenetically engineered mice and morphometric, transcriptomic, and functional analyses were used. Additionally, inflammatory mediators and bone turnover markers were measured in the serum of healthy controls, individuals with latent tuberculosis and patients with active tuberculosis.Results and discussionWe found that infection with Mycobacterium avium impacts bone turnover by decreasing bone formation and increasing bone resorption, in an IFNγ- and TNFα-dependent manner. IFNγ produced during infection enhanced macrophage TNFα secretion, which in turn increased the production of serum amyloid A (SAA) 3. Saa3 expression was upregulated in the bone of both M. avium- and M. tuberculosis-infected mice and SAA1 and 2 proteins (that share a high homology with murine SAA3 protein) were increased in the serum of patients with active tuberculosis. Furthermore, the increased SAA levels seen in active tuberculosis patients correlated with altered serum bone turnover markers. Additionally, human SAA proteins impaired bone matrix deposition and increased osteoclastogenesis in vitro. Overall, we report a novel crosstalk between the cytokine-SAA network operating in macrophages and bone homeostasis. These findings contribute to a better understanding of the mechanisms of bone loss during infection and open the way to pharmacological intervention. Additionally, our data and disclose SAA proteins as potential biomarkers of bone loss during infection by mycobacteria.

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Project description:Serum Amyloid A proteins reduce bone mass during mycobacterial infections

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Genetic Basis of Pulmonary Non-tuberculous Mycobacterial Infections

Project description:<p>This project aims at characterizing the human host susceptibility to pulmonary non-tuberculous mycobacterial (PNTM) infections. PNTM infections occur in patients with chronic lung disease, but also in a distinct group of elderly women without lung defects but who share a common body morphology: tall and lean with scoliosis, pectus excavatum, and mitral valve prolapse. We performed whole exome and genome sequencing in extended families of patients with active PNTM. This unique collection of familial cohorts in PNTM represents an important opportunity for a high yield search for genes that regulate mucosal immunity. We also sequenced the genome of mycobacterial isolates from PNTM patients to integrate host PNTM susceptibility with mycobacterial genotypes and gain insights into the key factors involved in this devastating disease.</p>

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The effects of Serum Amyloid A on gene expression profile in HUVECs

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