On the skin's surface, bacteria are abundant（丰富的，充裕的）, diverse（不同的，相异的） and constant（经常的，不变的）, but inflammation（发炎，红肿） is undesirable（不受欢迎的，不良的）. 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（严重发炎） 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 on November 22, was done in mice and in human cell cultures（细胞培养）, primarily performed by post-doctoral fellow Yu Ping Lai .

"The exciting implications of Dr. Lai's work is that it provides a molecular¹ basis to understand the 'hygiene² hypothesis（卫生假说）' and has uncovered elements of the wound repair response that were previously³ unknown. This may help us devise new therapeutic⁴（治疗的） 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（微生物） increases an individuals susceptibility（感受性，感情） to disease by changing how the immune system reacts to such "bacterial⁵ invaders⁶." The hypothesis was first developed to explain why allergies⁷ like hay fever（花粉热，干草热） and eczema（湿疹） were less common in children from large families, who were presumably（推测上，大概） exposed to more infectious agents than others. It is also used to explain the higher incidence（发生） of allergic⁸ diseases in industrialized countries.

The skin's normal microflora（微生物群落） – the microscopic⁹（显微镜的，微观 的） and usually harmless bacteria that live on the skin – includes certain staphylococcal（葡萄球菌） bacterial species that will induce an inflammatory response when they are introduced below the skin's surface, but do not initiate¹⁰ inflammation when present on the epidermis¹¹（表皮，上皮）, or outer layer of skin.

In this study, Lai, Gallo and colleagues reveal a previously unknown mechanism¹² by which a product of staphylococci（葡萄状球菌） inhibits¹³ skin inflammation. Such inhibition is mediated¹⁴ by a molecule¹⁵ called staphylococcal lipoteichoic acid（脂磷壁酸） (LTA) which acts on keratinocytes（角化细胞） – the primary cell types found on the epidermis.

The researchers also found that Toll-like receptor 3 (TLR3) activation¹⁶ 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（上皮，上皮细胞） requires TLR3 for normal inflammation after wounding and that the microflora helps to modulate¹⁷（调制） this response."