We hope that this week’s newsletter finds all of our readers safe and healthy. While not all the news we bring this week is joyous (for example, reports of significantly heightened stress among mothers of children with eczema), the week has been a motherlode of significant advancement of science across multiple fields. Newly-published studies on genetics, immunology, dermatology, neurology, and evolutionary biology give us a lot to think about over the upcoming week, and, we hope, some things to be optimistic about.
Atopic Dermatitis Treatment Update
Starting off in our favorite field! The American Academy of Dermatology (AAD) has updated its guidelines on topical treatments for adults with atopic dermatitis for the first time since 2014. These guidelines were developed by 12 physicians (11 dermatologists and one allergist) and a patient representative. The recommendations include the use of moisturizers and calcineurin inhibitors, among other things. With so many new biologic treatments emerging, you have to wonder what kinds of recommendations we’ll see nine or ten years from now!
Maternal Stress Caused By Eczema
In related news, it’s no secret that eczema is a source of stress, both for sufferers and for those tasked with their care. Many studies over the years have shown a strong correlation between pediatric eczema and maternal stress. A recent Korean study, published last week, found that rates of depression, stress, and even suicidal ideation affect mothers of children with eczema at higher rates than the general population; fathers of these children, meanwhile, experience the same mental health concern at the same rate as the general population.
Researchers point out that while atopic dermatitis is exacerbated by stress, the disorder itself generates tremendous stress. They also note that in Korean society, mothers provide almost all of the childcare within a family. Caring for a child with an uncomfortable, chronic disorder would therefore affect mothers disproportionately.
Skin and The Aging Process
While we’re on the topic of skin, have you ever wondered why our skin loses elasticity and begins to wrinkle as we age? Or why our hair goes grey? Aging has perplexed humanity since the dawn of time, as evidenced by the many quests for a “fountain of youth.” Six centuries after Ponce De Leon set out to find such a fountain in the Americas, the mechanisms of the aging process continue to elude our understanding.
Luís Amaral, a professor of chemical and biological engineering at Northwestern University, believes that he and his colleagues are closer to understanding the aging process better–what’s more, they have found that it is possible to limit or even reverse some effects of aging.
When Amaral and his team set out to examine age-related changes in gene expression, they found no consistent patterns; Amaral says, “It seemed like almost everything was random.”
That changed when the team began to examine the length of genes that were being expressed at different stages of life. In both mice and human tissues, they found that shorter genes are expressed more often while longer genes are expressed less often with age. Many of the shorter genes are associated with shortened lifespan, while many of the genes associated with longevity were found among the longest genes.
Amaral and his team went on to examine the effects of 12 antiaging interventions on the expression of both long and short genes. Of those interventions, seven–including anti aging drugs rapamycin and resveratrol–led to a relative increase in long-gene transcripts.
The root of this age-related imbalance between short genes and long genes, Amaral says, could lie with cumulative damage inflicted by exposures to harmful pathogens and toxins over time. Maybe aging can be measured, he says, by this imbalance. He acknowledges that factors other than transcription length may be at play; he hopes to study how injury might influence gene-length imbalance in younger bodies.
“We hope that this study will get people excited to do experiments that could help us unravel what’s going on in greater depth,” he says.
While it isn’t a miraculous fountain of youth, their work could provide a springboard for the development of therapies for age-related disorders.
T-Cells and the Immune System
T-cells are frequently regarded as the adaptive immune system all-stars; they are important to the generation of antigen-specific antibodies.An article published recently in Nature Immunology reveals that some subsets of helper T cells have a few surprising tricks up their sleeves.
The European study cited by the article found that certain subsets of Th17 cells produce interleukin α (IL-1α), a powerful pro-inflammatory cytokine closely associated with the innate immune system.
Calling it “a signal molecule for danger,” Zielinski says that “even the smallest amounts are enough to trigger fever.”
Interleukin 1α is abundant in both epithelial and endothelial tissues, making it one of the first responders when a foreign antigen is encountered. Until the European study, however, no one was aware that Th17 cells could produce this cytokine. Interleukin 1α is produced by a diverse set of proteins within the Th17 cells called an inflammasome; inflammasomes were not known to exist within T cells prior to this.
The Th17 cells had more surprises for Zielinski and her fellow researchers. The cytokine exits the Th17 cells through pores made in the cell walls by a molecule called gasdermin e.
Gasdermins are best known as effectors of pre-programmed cell death, penetrating the cell membrane of cells to kill them. This is the first time researchers have seen gasdermin pores acting to deliver pro-inflammatory molecules from within a T cell.
The Th17 cells are important to the body’s defense against fungal infection, most especially against the candida genus. Zielinski suspects that the cytokine-secreting cells are part of that specialized defense.
Neuropathic Pain Mechanism Improvements
We conclude our weekly update with some good news for people suffering with neuropathic pain. Neuropathic pain is not well-understood, and it is difficult to treat; in fact, treatments for neuropathy were all originally formulated to treat depression and/or epilepsy. Yet after ten years of research, Brazilian scientists have found a mechanism of neuropathic pain. Even better, they predict that this discovery will soon yield viable treatments for neuropathic pain.
Neuropathic pain is chronic, and it is often experienced as sharp, stabbing sensations. It arises from damage to the nervous system caused by injury or illness. The Brazilian study identified an inflammatory response beginning with dendritic cells (an immune cell) found in the meninges (the membrane that covers the spinal cord and brain). Inflammatory responses in these cells after injury lead to an excess production of an enzyme called IDO1 (indoleamine 2,3-dioxygenase 1), which in turn leads to increased production of kynurenine (a by-product of the metabolism of tryptophan).
By inhibiting the production of kynurenine with the pharmaceutical or genetic treatment, the researchers found that they could successfully nullify neuropathic pain.
The Brazilian study could bear fruit well beyond the treatment of neuropathy; dysregulation of kynurenine production and metabolism is a feature of depression and schizophrenia, as well.
What an eventful week! We hope this week’s news provided a bright spot amid news of loosened krakens, egg shortages, and disastrous weather. Take care of yourselves–moisturize regularly, stay hydrated, and stay tuned for more news next week.- Zula Elwood