This student story was published as part of the 2026 NASW Perlman Virtual Mentoring Program organized by the NASW Education Committee, providing science journalism experience for undergraduate and graduate students.
Story by Emmanuel Leon Colon Mentored and edited by Michael E. Newman
If you’ve ever been bitten by a mosquito, then you’re very familiar with the discomfort those small red bumps give you for a few hours. That’s because the mosquito’s saliva releases chemicals into your bloodstream that in turn, trigger immune system cells to release inflammatory messengers resulting in localized swelling and itching. Now imagine if you had to feel something similar for years on end because of an overactive and faulty immune system causing persistent skin inflammations.
Chronic inflammatory skin disorders are a group of diseases that cause excessive itch, pain, swelling and sometimes, scarring, due to the immune system mistakenly seeing healthy tissues as harmful. Some examples of these disorders include psoriasis, lupus and scleroderma; and most cause a significant decrease in a patient’s quality of life.
Normally, the immune system acts as the body’s surveillance and protection system. Just like security guards patrolling a shopping mall, the immune system is constantly moving through the body, looking for foreign invaders and adverse substances, like the chemicals coming from mosquito bites.
In the skin, immune cells detect these hazards and recruit more immune cells to support the attack in the same way security guards call the police for backup. Recent research has uncovered that neurons of the skin are just as capable of triggering skin inflammation by talking directly to the immune system.
Neurons are the cells of the nervous system with body-wide projections that allow them to sense external signals such as temperature, odors, pressure and mechanical stimulation. Dan Kaplan, a dermatologist, immunologist and physician-scientist at the University of Pittsburgh, has been studying how neurons maintain inflammation and how they might be leveraged to treat chronic inflammatory skin disorders.
“For a long time there has been anecdotal evidence that people who have damaged skin neurons develop increased infections, but when they are inhibited in the context of inflammatory skin diseases, their disease spontaneously resolves” said Kaplan.
For example, Kaplan learned about a case study about a patient with psoriasis in both arms who dislocated their right shoulder. Temporarily cutting off the signals generated by the neurons in that arm led to remission of most of the psoriatic plaques there, while the left arm remained diseased.
“We’ve seen similar results when injecting botulinum toxin, more commonly known as Botox, into plaques of psoriasis and atopic dermatitis,” Kaplan said. “Botox suppresses nerve transmissions and lessens the immune response that leads to chronic inflammation.”
Kaplan’s research has found that skin neurons trigger the release of protein-destroying enzymes called proteases from a type of white blood cell known as a mast cell. Proteases include substances such as the blood thinner heparin and the allergic stimulant histamine (the same histamine blocked by many allergy medications), with inflammation and skin irritation as side effects.
Kaplan and his colleague studied mice genetically grown to lack mast cells that there were significant reductions in skin inflammation, possibly because there was no histamine present as well.
Based on several previous studies linking skin neurons to inflammation, Kaplan’s group is exploring which chemical compounds could be used to block that connection, stop the neurons from activating mast cells to release inflammatory agents, and potentially become treatments for chronic inflammatory skin disorders.
One such chemical that Kaplan and his group believe has promise is beta-alanine, an amino acid used in many pre-workout supplements. The researchers observed that beta-alanine stimulates skin neurons to produce glutamic acid, an anti-inflammatory amino acid, that in turn, shuts down activated mast cells and inhibits inflammation.
This finding has led Kaplan and his colleagues to begin clinical research to determine the effectiveness of beta-alanine in treating chronic inflammatory skin disorders.
“The promise is that if you understand how these inflammatory nerves are promoting skin disease, there are a number of strategies that you can target without resorting to current approaches using immunosuppressant drugs,” Kaplan said.
Such therapies, while effective in treating skin inflammation, can leave patients vulnerable to more serious infections and even cancers because they result in an underactive immune system.
If researchers like Kaplan can find ways to successfully manipulate the nerve signals that trigger chronic inflammatory skin disorders, there may soon be a much-needed improvement in the quality of life for patients who suffer from them.
Main header image caption: A photomicrograph showing an activated mastocyte (mast cell) at the center surrounded by osteocytes (bone cells). Credit: Public domain image via Wikimedia Commons.
Emmanuel Leon Colon holds a masters degree in immunology from the University of Pittsburgh where he studied memory T cells and how they protect the gastrointestinal tract. He is fascinated by the emerging field of neuroimmune interactions where scientists study how the immune system and the nervous system communicate with each other to drive host defense and normal body maintenance.
The NASW Perlman Virtual Mentoring program is named for longtime science writer and past NASW President David Perlman. Dave, who died in 2020 at the age of 101 only three years after his retirement from the San Francisco Chronicle, was a mentor to countless members of the science writing community and always made time for kind and supportive words, especially for early career writers.
You can contact the NASW Education Committee at education@nasw.org. Thank you to the many NASW member volunteers who lead our #SciWriStudent programming year after year.
Founded in 1934 with a mission to fight for the free flow of science news, NASW is an organization of ~ 2,300 professional journalists, authors, editors, producers, public information officers, students and people who write and produce material intended to inform the public about science, health, engineering, and technology. To learn more, visit www.nasw.org
