Researchers ID How Skin Ages, Loses Fat and Immunity

This is a microscopic image of the skin reveals skin cells in blue and fat cells in green. The fat cell layer forms the final barrier against bacteria entering deep into the body. (Photo courtesy of UC San Diego Health)

Pictured here is a microscopic image of the skin reveals skin cells in blue and fat cells in green. The fat cell layer forms the final barrier against bacteria entering deep into the body. (Photo courtesy of UC San Diego Health)

University of California San Diego School of Medicine researchers and colleagues show how fibroblasts develop into fat cells and identify the pathway that causes this process to cease as people age. The study was published in Immunity.

“We have discovered how the skin loses the ability to form fat during aging,” says Richard Gallo, MD, PhD, distinguished professor and chair of the Department of Dermatology at UC San Diego School of Medicine and senior author on study.

“Loss of the ability of fibroblasts to convert into fat affects how the skin fights infections and will influence how the skin looks during aging,” he adds.

Gaining weight isn’t the path to converting dermal fibroblasts into fat cells since obesity also interferes with the ability to fight infections. Instead, a protein that controls many cellular functions, called transforming growth factor beta (TGF-β), stops dermal fibroblasts from converting into fat cells and prevents the cells from producing the antimicrobial peptide cathelicidin, which helps protect against bacterial infections, reported researchers, a media release from University of California – San Diego explains.

“Babies have a lot of this type of fat under the skin, making their skin inherently good at fighting some types of infections. Aged dermal fibroblasts lose this ability and the capacity to form fat under the skin,” Gallo adds. “Skin with a layer of fat under it looks more youthful. When we age, the appearance of the skin has a lot to do with the loss of fat.”

In mouse models, researchers used chemical blockers to inhibit the TGF-β pathway, causing the skin to revert back to a younger function and allowing dermal fibroblasts to convert into fat cells. Turning off the pathway in mice by genetic techniques had the same result.

Understanding the biological process that leads to an age-dependent loss of these specialized fat cells could be used to help the skin fight infections like Staphylococcus aureus (S. aureus) — a pathogenic bacteria that is the leading cause of infections of the skin and heart and a major factor in worsening diseases, like eczema. When S. aureus becomes antibiotic resistant it is known as methicillin-resistant Staphylococcus aureus or MRSA, which is a leading cause of death resulting from infection in the United States.

The long-term goals and benefits of this research are to understand the infant immune system, Gallo states. The results may also help understand what goes wrong in other diseases like obesity, diabetes, and autoimmune diseases, per the release.

[Source(s): University of California – San Diego, EurekAlert]