Yu Ping Laiによる研究によれば、傷害に対する細胞の炎症反応を抑制する細菌からの科学的シグナルを受ける特別な受容体を皮膚細胞が持っているという。ケラチノサイトという細胞は、正常な炎症性免疫反応を生成するためにToll-like receptor 3 という受容体からのシグナルを受け取る必要がある。細菌が作るstaphylococcal lipoteichoic acid という化学物質が受容体を活性化するのを抑制している。しかし、表皮より深くまで傷害されると、もっと強力な免疫反応が作り出されて傷が癒える。
Eek! Our Skin Is Full Of Bugs
But researchers say that so-called microflora is good for our health.
By Jonathan Fahey, Forbes
No matter how much yogurt we eat or kambucha we drink, no matter how much we hear about how bacteria can be beneficial to us, it still can seem creepy that there are up to 1,000 species of bacteria and fungi lounging around on our skin at any given time--1 trillion or so microscopic residents.
Maybe new research that shows just how one of our many freeloaders pays a little rent will help. It turns out certain species of staphylococcal bacteria help the skin regulate its immune response to injury and ward off disease.
It has long been known that our skin teems with so-called microflora. Earlier research has revealed how many species there are (somewhere between 300 and 1,000), where most thrive best (the forearm) and worst (behind the ear). We know that our good bacteria crowd out pathogenic bacteria and that some even secrete a natural antibiotic to ward off these bad bacteria and secure more space for themselves.
We haven't, though, understood whether or how species work with our bodies to help us. But new research out of the lab of Richard Gallo, professor of medicine and pediatrics and the chief of University of California at San Diego's Division of Dermatology, reveals a tight relationship between staphylococcal bacteria and cells on the outer layer of skin, or epidermis.
The research also offers some biological evidence to support the theory that humans in industrialized nations are more susceptible to certain diseases and allergies because they aren't exposed enough to micro-organisms, especially early in life.
The work, performed by post-doctoral fellow Yu Ping Lai and published in the journal Nature Medicine, shows that skin cells have special receptors that pick up chemical signals from the bacteria that inhibit the cells' inflammatory response to injury.
These cells, called keratinocytes, must receive signals from a receptor called Toll-like receptor 3 in order to generate the normal inflammatory immune response. A chemical produced by the bacteria called staphylococcal lipoteichoic acid prevents the receptor from being activated.
This isn't the case for cells in skin layers below the epidermis, however, so if the cut is deep enough, a more powerful immune response is produced, and we heal.
"Too little inflammation is bad, and too much inflammation is bad," says Gallo.
"What's beautiful about this system is that if the [skin] barrier isn't broken we inhibit inflammation, but if it is broken, we allow inflammation to occur."
Gallo suspects that this system may be upset in patients who suffer from eczema, a disease that involves excessive inflammation. And studies have shown that people with eczema get worse when they move to industrialized nations where, presumably they are exposed to fewer micro-organisms.
This creates a puzzle, though. When we wash our hands to remove pathogens, we are also removing bacteria that can help protect us against those same pathogens as well as other diseases. What should we do?
"Right now, we know absolutely that we need to get rid of the pathogens; hand washing protocols need to be maintained," says Gallo. "The goal would be to develop a hand washing technique that would kill pathogens but leave beneficial bacteria alone."
That would mean developing an anti-bacterial soap that kills only certain bacteria--a tall order. In the meantime, Gallo would like to explore the links between his findings and diseases like eczema and try to understand how other bugs on our skin may help us.
"My suspicion is that we'll find other beneficial roles for other microflora if we keep looking," he says.
So as you curl up in bed tonight, think about the trillion tiny, thriving, vigorous bugs that are nestling with you all over your skin. They're there to help you. Really.
Commensal bacteria regulate Toll-like receptor 3|[ndash]|dependent inflammation after skin injury
Yuping Lai , Anna Di Nardo , Teruaki Nakatsuji , Anke Leichtle , Yan Yang , Anna L Cogen , Zi-Rong Wu , Lora V Hooper , Richard R Schmidt , Sonja von Aulock , Katherine A Radek , Chun-Ming Huang , Allen F Ryan & Richard L Gallo
The normal microflora of the skin includes staphylococcal species that will induce inflammation when present below the dermis but are tolerated on the epidermal surface without initiating inflammation. Here we reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. This inhibition is mediated by staphylococcal lipoteichoic acid (LTA) and acts selectively on keratinocytes triggered through Toll-like receptor 3(TLR3). We show that TLR3 activation is required for normal inflammation after injury and that keratinocytes require TLR3 to respond to RNA from damaged cells with the release of inflammatory cytokines. Staphylococcal LTA inhibits both inflammatory cytokine release from keratinocytes and inflammation triggered by injury through a TLR2-dependent mechanism. To our knowledge, these findings show for the first time that the skin epithelium requires TLR3 for normal inflammation after wounding and that the microflora can modulate specific cutaneous inflammatory responses.
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