Obesity: What does immunity have to do with it?
New findings may represent a promising approach for obesity treatment and
its complications

Date:
February 22, 2022
Source:
Boston University School of Medicine
Summary:
As organisms grow, older cells can undergo a phenomenon called
senescence. This process defines a cell state where cells
permanently stop dividing but do not die. Senescent cells secrete
toxic pro- inflammatory factors contributing to the development
of many diseases.

Researchers from Boston University School of Medicine (BUSM)
have shown that obesity in experimental models led to senescence
of macrophages, an immune cell subtype within fat or adipose tissue.



FULL STORY ==========================================================================
As organisms grow, older cells can undergo a phenomenon called
senescence. This process defines a cell state where cells permanently stop dividing but do not die. Senescent cells secrete toxic pro-inflammatory
factors contributing to the development of many diseases.


========================================================================== Researchers from Boston University School of Medicine (BUSM) have shown
that obesity in experimental models led to senescence of macrophages,
an immune cell subtype within fat or adipose tissue.

According to the researchers, the fact that macrophages can become
senescent is an unexpected finding. Many of the macrophages within obese
tissue were senescent and those senescent cells may be a significant
driver of fat tissue fibrosis. These findings suggest that obesity
accelerates cellular or biological immune aging in fat.

"In healthy individuals, those cells contribute to cleaning the tissue
from dead adipocytes (cells specialized for the storage of fat) and help
in the cellular turnover. We demonstrated that macrophages lost this
capacity when they become senescent," explained first and co-corresponding author Nabil Rabhi, PhD, an instructor of biochemistry at BUSM.

The researchers also found that senescent macrophages secrete a variety of factors, one of which is a molecule called osteopontin which they found
is responsible for adipose tissue fibrosis. "Our finding suggests that macrophages ages faster in obese animals. This accelerated senescence
may contribute to the pathological thickness or fibrosis of fat tissue
observed in obese individuals with type 2 diabetes," said Rabhi. The researchers believe understanding new regulatory pathways that control
adipose tissue responses to obesity may help identify new targets for
obesity treatment. "Our finding indicates that targeting the senescent macrophages population or using osteopontin inhibition may represent a promising approach for obesity treatment and its adverse complication
including type 2 diabetes," added Rabhi.

Collaborators from BUSM included co-corresponding authors Matthew
D. Layne, PhD, associate professor of biochemistry and assistant dean
for research and Stephen R. Farmer, PhD, professor of biochemistry.

These findings appear online in the journal Life Science Alliance.

Funding for this study was provided by the National Institutes of Health/ National Institute of Diabetes and Digestive and Kidney Diseases (DK117161
and DK117163 to SRF), the American Heart Association (AHA) fellowship (17POST33660875 to NR) and The Evans Center for Interdisciplinary
Biomedical Research ARC on "Connecting Tissues and Investigators,
Fibrosis in Pathology" at Boston University.

========================================================================== Story Source: Materials provided by
Boston_University_School_of_Medicine. Note: Content may be edited for
style and length.


========================================================================== Journal Reference:
1. Nabil Rabhi, Kathleen Desevin, Anna C Belkina, Andrew Tilston-Lunel,
Xaralabos Varelas, Matthew D Layne, Stephen R
Farmer. Obesity-induced senescent macrophages activate a fibrotic
transcriptional program in adipocyte progenitors. Life Science
Alliance, 2022; 5 (5): e202101286 DOI: 10.26508/lsa.202101286 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2022/02/220222121240.htm

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