Vuil is goed
voor de huid*
Vuil is goed voor de huid ook bij kinderen, zij mogen best wel eens smerig worden, aldus Amerikaanse wetenschappers. Als je te schoon bent, vermindert dat het vermogen van de huid zichzelf te herstellen.
Normale bacteriën die op de huid leven, brengen een kettingreactie teweeg, die helpt een ontsteking te voorkomen als we gewond raken. Zij temperen overactieve reacties van het immuunsysteem, die sneetjes en schrammen laten zwellen.
De stafylokok-bacteriën blokkeren een vitale stap in een reeks gebeurtenissen die tot een ontsteking leiden, concludeerden deskundigen van de Universiteit van Californië in San Diego. Zij publiceerden hun bevindingen in
Nature Medicine.
Volgens deskundigen levert het onderzoek een verklaring voor de zogenoemde hygiëne-hypothese, die stelt dat blootstelling aan bacteriën in de vroege kinderjaren het lichaam wapent tegen allergieën.
De obsessie met reinheid zou zelfs een oorzaak kunnen zijn voor de recente stijging van allergieën in ontwikkelde landen.
Surface Bacteria Maintains
Skin’s Healthy Balance
On the skin’s surface, bacteria are abundant, diverse and constant, but inflammation is undesirable. Research at the University of California, San Diego School of Medicine now shows that the normal bacteria living on the skin surface trigger a pathway that prevents excessive inflammation after injury.
“These germs are actually good for us,” said Richard L. Gallo, MD, PhD, professor of medicine and pediatrics, chief of UCSD’s Division of Dermatology and the Dermatology section of the Veterans Affairs San Diego Healthcare System.
The study, to be published in the advance on-line edition of Nature Medicine, was done in mice and in human cell cultures, primarily performed by post-doctoral fellow Yu Ping Lai .
“The exciting implications of Dr. Lai’s work is that it provides a molecular basis to understand the ‘hygiene hypothesis’ and has uncovered elements of the wound repair response that were previously unknown. This may help us devise new therapeutic approaches for inflammatory skin diseases,” said Gallo.
The so-called “hygiene hypothesis,” first introduced in the late 1980s, suggests that a lack of early childhood exposure to infectious agents and microorganisms increases an individuals susceptibility to disease by changing how the immune system reacts to such “bacterial invaders.” The hypothesis was first developed to explain why allergies like hay fever and eczema were less common in children from large families, who were presumably exposed to more infectious agents than others. It is also used to explain the higher incidence of allergic diseases in industrialized countries.
The skin’s normal microflora – the microscopic and usually harmless bacteria that live on the skin – includes certain staphylococcal bacterial species that will induce an inflammatory response when they are introduced below the skin’s surface, but do not initiate inflammation when present on the epidermis, or outer layer of skin.
In this study, Lai, Gallo and colleagues reveal a previously unknown mechanism by which a product of staphylococci inhibits skin inflammation. Such inhibition is mediated by a molecule called staphylococcal lipoteichoic acid (LTA) which acts on keratinocytes – the primary cell types found on the epidermis.
The researchers also found that Toll-like receptor 3 (TLR3) activation is required for normal inflammation after skin injury.
“Keratinocytes require TLR3 to mount a normal inflammatory response to injury, and this response is kept from becoming too aggressive by staphylococcal LTA,” said Gallo. “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 helps to modulate this response.”
Additional contributors to the paper include Yuping Lai, Anna Di Nardo, Teruaki Nakatsuji, Anna L Cogen, Chun-Ming Huang and Katherine A. Radek, UCSD Division of Dermatology and the VA San Diego Healthcare System; Anke Leichtle and Allen F. Ryan, UCSD Department of Surgery/Otolaryngology and the VA San Diego Healthcare System; Yan Yang and Zi-Rong Wu, School of Life Science, East China Normal University, Shanghai; Lora V Hooper, Howard Hughes Medical Institute and University of Texas Southwestern Medical Center, Dallas; and Richard R Schmidt and Sonja von Aulock, University of Konstanz, Germany.
The study was funded by grants from the National Institutes of Health, and a US Veterans Administration Merit
Award.
Abstract
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. (November
2009)
