Tuberculosis induces premature cellular aging
Date:
March 24, 2022
Source:
Baylor College of Medicine
Summary:
Researchers found that the cells of humans and animals who have
recovered from tuberculosis had prematurely aged up to 12 to 14
years. It's possible that this premature cellular aging is one
reason why survivors of tuberculosis have a high risk of mortality.
FULL STORY ========================================================================== Tuberculosis (TB) is a potentially serious infectious disease caused
by a type of bacterium called Mycobacterium tuberculosis. The bacteria
usually affect the lungs, but also can invade other organs.
==========================================================================
In 2018, tuberculosis bacteria infected 1.7 billion people -roughly 23%
of the world's population, according to the Centers for Disease Control
and Prevention (CDC). In 2020, the CDC reported 7,174 TB cases and 13
million people living with a latent tuberculosis infection (the germs
are in the body but do not cause sickness) in the United States.
Even after successful therapy for tuberculosis, survivors of the disease
have an increased risk of recurrent infection and death. A new study
published recently by researchers at Baylor College of Medicine found
that the cells of humans and animals who have recovered from tuberculosis
had prematurely aged up to 12 to 14 years.
"It's possible that this premature cellular aging is one reason why
survivors of tuberculosis have a high risk of mortality," said Dr. Andrew DiNardo, assistant professor of infectious diseases at Baylor College
of Medicine and senior author of the paper.
To measure the aging of the cells, researchers looked at the epigenetic
clock of the cells. Epigenetics looks at how the DNA inside every cell
is coiled. As we age, how the DNA is coiled changes, and severe infection
is changing it in such a way to increase premature aging.
In this study, the researchers studied multiple cohorts and multiple
tissue types, and discovered that tuberculosis induced perturbations in epigenetic regulation, specifically in the regulation mediated by DNA methylation. These changes correlated with oxidative stress-induced
senescence and was associated with premature cellular aging. These
processes were conserved across both guinea pigs and humans.
========================================================================== DiNardo, who also is with Texas Children's Hospital, says that this is an important area to look into after any severe infection, including sepsis
or even SARS-CoV-2. The severity of the infection also could play a role
in the aging of the cells.
"A multi-omic epigenetic clock assay could become part of the standard
of care for infectious diseases and further inform increased risk for comorbidities after chronic conditions or environmental exposure,"
said Dr. Cristian Coarfa, associate professor of molecular and cellular
biology at Baylor and co- corresponding author of the paper. Coarfa also
is with the Dan L Duncan Comprehensive Cancer Center at Baylor.
A multi-omic approach would integrate epigenomics and other 'omics,' such
as proteomics (proteins produced), metabolomics (metabolites present)
and microbiomics (microorganisms) data.
"Now that we know the mechanism, there are some ways that we can target
it to slow down and decrease the premature epigenetic aging that is
happening in these cells," Coarfa said.
Their report appears in the journal Aging.
Others who took part in the study include Carly A. Bobak, Abhimanyu,
Harini Natarajan, Tanmay Gandhi, Sandra L. Grimm, Tomoki Nishiguchi,
Kent Koster, Santiago Carrero Longlax, Qiniso Dlamini, Jacquiline Kahari, Godwin Mtetwa, Jeffrey D. Cirillo, James O'Malley and Jane E. Hill. The
authors are affiliated with one or more of the following institutions:
Geisel School of Medicine at Dartmouth College, Texas Children's
Hospital, the Dan L Duncan Comprehensive Cancer Center at Baylor,
Texas A&M University Health, Baylor-Swaziland Children's Foundation and University of British Columbia.
This work was supported by NIAID K23 AI141681-02, partially by the Cancer Prevention Institute of Texas (CPRIT) RP170005, RP210227, and RP200504,
NIH P30 shared resource grant CA125123, and NIEHS grants 1P30ES030285
and 1P42ES027725.
Further support was provided by the Texas A&M University System and
National Institutes of Health grants AI104960 and AI149383, NHLBI R01, HL146228-01, the Cystic Fibrosis Foundation Hill18A0-CI, the National
Science and Engineering Research Council, Canada, AWD-01777,3 and the
National Health, the Medical Research Council, Australia GNT1182929,
Burroughs Wellcome Fund institutional program grant to Dartmouth College (Grant#1014106).
========================================================================== Story Source: Materials provided by Baylor_College_of_Medicine. Original written by Dipali Pathak. Note: Content may be edited for style and
length.
========================================================================== Journal Reference:
1. Carly A. Bobak, Abhimanyu, Harini Natarajan, Tanmay Gandhi,
Sandra L.
Grimm, Tomoki Nishiguchi, Kent Koster, Santiago Carrero Longlax,
Qiniso Dlamini, Jacquiline Kahari, Godwin Mtetwa, Jeffrey
D. Cirillo, James O'Malley, Jane E. Hill, Cristian Coarfa,
Andrew R. DiNardo. Increased DNA methylation, cellular senescence
and premature epigenetic aging in guinea pigs and humans with
tuberculosis. Aging, 2022; 14 (5): 2174 DOI: 10.18632/aging.203936 ==========================================================================
Link to news story:
https://www.sciencedaily.com/releases/2022/03/220324130315.htm
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