Tuberculosis survivors must combat the risk of premature cellular senescence, recurrent tuberculosis infection and death: US study

Tuberculosis or tuberculosis causes premature aging of cells, causes recurrent infections, and can lead to premature death-showing a study by Baylor College of Medicine, USA.

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Washington: New research by researchers Baylor College of Medicine Human and animal cells recovered from tuberculosis He was aging prematurely between the ages of 12 and 14.

The results of the study were published in the journal “Aging”.

Even after successful treatment of tuberculosis, tuberculosis survivors are at increased risk of recurrent infection and death.

“This is possible Early cellular senescence This is one of the reasons why tuberculosis survivors are at high risk of death, “said Dr. Andrew Dinaldo, an assistant professor of infectious diseases at Baylor College of Medicine and lead author of the treatise.

To measure cell aging, researchers examined the epigenetic clock of cells. Epigenetics examines how the DNA in every cell is coiled. As we age, how DNA is coiled changes, and severe infections change DNA in ways that increase premature aging.

In this study, researchers studied multiple cohorts and multiple tissue types, resulting in tuberculosis. Epigenetic regulationEspecially in regulation mediated by DNA methylation. These changes correlated with oxidative stress-induced aging and were associated with premature cellular senescence. These processes were conserved in both guinea pigs and humans.

Dinaldo, who also belongs to the Texas Children’s Hospital, says this is an important area to look for after severe infections, including sepsis and SARS-CoV-2. The Severity of infection It can also play a role in cell aging.

“Multi-omic Epigenetic clock assay Dr. Christian Koafa, an associate professor of molecular and cell biology at Baylor University and co-author of the treatise, said:

The multi-omic approach integrates epigenomics with other “omics”. Proteomics Data on (protein produced), metabolomics (with metabolites) and microbial flora (microorganisms).

“Once we know the mechanism, there are several ways we can target it to delay and reduce the premature epigenetic aging that is occurring in these cells,” Coarfa concludes. (ANI)

(The article was created by ANI. Only the headline has changed.)

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