Surface Bacteria Maintain the Skin's Healthy Balance

A new study has found that bacteria living on the skin surface trigger a pathway that prevents excessive inflammation after injury.

Researchers from the University of California, San Diego (UCSD; USA) conducted a study in mice and in human cell cultures that revealed a previously unknown mechanism by which staphylococcal lipoteichoic acid (LTA)--a product of staphylococcal bacteria--inhibits skin inflammation by acting on keratinocytes, the primary cell types found on the epidermis. The researchers found that staphylococcal LTA controls the skin keratinocytes response by modulating toll-like receptor 3 (TLR3) activation, which is needed by the cells to mount a normal inflammatory response to injury. The study, which was primarily performed by postdoctoral fellow Yu Ping Lai, was published on November 22, 2009, in the advance on-line edition of Nature Medicine.

"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,” said senior author Professor Richard Gallo, M.D., Ph.D., a professor of medicine and pediatrics and chief of UCSD's division of dermatology. "The exciting implication of the 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.”

The hygiene hypothesis, first introduced in the late 1980's, suggests that a lack of early childhood exposure to infectious agents and microorganisms increases an individuals susceptibility to disease by changing the way 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.

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