No More Needles: Stanford Scientists Create a Painless, Living Vaccine You Rub on Your Skin – SciTechDaily
Source: SciTechDaily
Stanford scientists discovered that a harmless skin bacterium triggers a powerful immune response. By tweaking a bacterial protein, they turned it into a living vaccine, training the immune system to fight diseases like tetanus and diphtheria.
Mice given this bioengineered bacterium developed strong immunity, surviving lethal toxin doses. With human trials on the horizon, this could revolutionize vaccination—topical, painless, and highly effective.
Imagine a world where getting vaccinated is as simple as rubbing a cream onto your skin—no needles, no pain, and no unpleasant side effects like fever, swelling, or soreness. No long lines at the clinic, and best of all, it’s affordable.
Thanks to researchers at Stanford University, that future may be closer than we think. By harnessing a common skin bacterium found on nearly everyone, scientists are exploring a revolutionary approach to vaccination.
“We all hate needles — everybody does,” said Michael Fischbach, PhD, the Liu (Liao) Family Professor and a professor of bioengineering. “I haven’t found a single person who doesn’t like the idea that it’s possible to replace a shot with a cream.”
Surprisingly, the human skin is a harsh environment for most microbes, according to Fischbach. “It’s incredibly dry, way too salty for most single-celled creatures and there’s not much to eat. I can’t imagine anything would want to live there.”
But a few hardy microbes call it home. Among them is Staphylococcus epidermidis, a generally harmless skin-colonizing bacterial species.
“These bugs reside on every hair follicle of virtually every person on the planet,” Fischbach said.
Immunologists have perhaps neglected our skin-colonizing bacteria, Fischbach said, because they don’t seem to contribute much to our well-being. “We’ve just assumed there’s not much going on there.”
That turns out to be wrong. In recent years, Fischbach and his colleagues have discovered that the immune system mounts a much more aggressive response against S. epidermidis than anyone expected.
In a study published recently in Nature, Fischbach and his colleagues zeroed in on a key aspect of the immune response — the production of antibodies. These specialized proteins can stick to specific biochemical features of invading microbes, often preventing them from getting inside of cells or traveling unmolested through the bloodstream to places they should not go. Individual antibodies are extremely picky about what they stick to. Each antibody molecule typically targets a particular biochemical feature belonging to a single microbial species or strain.
Fischbach and postdoctoral scholar Djenet Bousbaine, PhD, respectively the study’s senior and lead author, and their colleagues wanted to know: Would the immune system of a mouse, whose skin isn’t normally colonized by S. epidermidis, mount an antibody response to that microorganism if it were to turn up there?
The initial experiments, performed by Bousbaine, were simple: Dip a cotton swab into a vial containing S. epidermidis. Rub the swab gently on the head of a normal mouse — no need to shave, rinse, or wash its fur — and put the mouse back in its cage. Draw blood at defined time points over the next six weeks, asking: Has this mouse’s immune system produced any antibodies that bind to S. epidermidis?
The mice’s antibody response to S. epidermidis was “a shocker,” Fischbach said. “Those antibodies’ levels increased slowly, then some more — and then even more.” At six weeks, they’d reached a higher concentration than one would expect from a regular vaccination — and they stayed at those levels.
“It’s as if the mice had been vaccinated,” Fischbach said. Their antibody response was just as strong and specific as if it had been reacting to a pathogen.
“The same thing appears to be occurring naturally in humans,” Fischbach said. “We got blood from human donors and found that their circulating levels of antibodies directed at S. epidermidis were as high as anything we get routinely vaccinated against.”
That’s puzzling, he said: “Our ferocious immune response to these commensal bacteria loitering on the far side of that all-important anti-microbial barrier we call our skin seems to have no purpose.”
What’s going on? It could boil down to a line scrawled by early-20th-century poet Robert Frost: “Good fences make good neighbors.” Most people have thought that fence was the skin, Fischbach said. But it’s far from perfect. Without help from the immune system, it would be breached very quickly.
“The best fence is those antibodies. They’re the immune system’s way of protecting us from the inevitable cuts, scrapes, nicks, and scratches we accumulate in our daily existence,” he said.
While the antibody response to an infectious pathogen begins only after the pathogen invades the body, the response to S. epidermidis happens preemptively, before there’s any problem. That way, the immune system can respond if necessary — say, when there’s a skin break and the normally harmle
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