Health
Tuberculosis disrupts epigenetic processes and promotes premature cell aging
Tuberculosis (TB) is a potentially serious infection caused by a type of so-called bacterium. Mycobacterium tuberculosis.. Bacteria usually affect the lungs, but they can also invade other organs.
In 2018, M. tuberculosis infected 1.7 billion people – – According to the Centers for Disease Control and Prevention (CDC), it accounts for about 23% of the world’s population. In 2020, the CDC reported 7,174 TB cases and 13 million people living in the United States with a latent tuberculosis infection (bacteria are present in the body but do not cause disease).
Even after successful treatment of tuberculosis, tuberculosis survivors are at increased risk of recurrent infection and death. A new study recently published by researchers at Baylor College of Medicine found that human and animal cells that recovered from tuberculosis age early to age 12-14.
This premature cellular senescence may be one of the reasons why tuberculosis survivors are at high risk of death. “
Dr. Andrew Dinaldo, 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 and found that tuberculosis induces perturbations in epigenetic regulation, especially those 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 the infection can also affect cell aging.
Dr. Christian Koafa, an associate professor of molecular and cell biology at Baylor University, said: Co-author of the treatise. Coarfa is also a member of Baylor’s Dan L Duncan Comprehensive Cancer Center.
The multi-omics approach integrates epigenomics with other “omics” such as proteomics (the protein produced), metabolomics (where metabolites are present), and microbial flora (microbial) data.
“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 said.
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Journal reference:
Bobak, California, et al. (2022) Increased DNA methylation, cellular senescence and premature epigenetic aging in guinea pigs and tuberculosis humans. aging. doi.org/10.18632/aging.203936..
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