Suppression of innate immunity by a nasal carriage strain of Staphylococcus aureus increases its colonization on nasal epithelium.
Suppression of innate immunity by a nasal carriage strain of Staphylococcus aureus increases its colonization on nasal epithelium.
复制标题
金黄色葡萄球菌鼻携带菌株对先天免疫的抑制增加了其在鼻上皮上的定植。
DOI：
10.1111/j.1365-2567.2007.02615.x
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发表时间：
2007
期刊：
影响因子：
6.4
通讯作者：
Cole,AlexanderM
中科院分区：
文献类型：
--
作者：
Quinn,GerryA;Cole,AlexanderM
Nasal carriage ofStaphylococcus aureusis an important source of nosocomial infection and community‐acquired methicillin‐resistantS. aureus(MRSA). Previous studies by our laboratory revealed that nasal carriage ofS. aureusis accompanied by subclinical inflammation, which is insufficient to prevent colonization, and that carriage might also be a result of adaptation and selection of certainS. aureusstrains to the host's nasal environment. In the present study we observed that a carrier strain ofS. aureuspreferentially colonizes and attaches to nasal epithelial cells (NEC) compared to a non‐carrierS. aureusstrain. Conversely, when naive NEC were pretreated with interleukin‐1β for 24 hr, the growth and attachment of the carrier strain ofS. aureuswere significantly reduced in comparison to the non‐carrier strain, emphasizing the pivotal role played by host innate immunity in the initial events of nasal carriage. While both strains up‐regulated the expression of the pattern recognition receptor, Toll‐like receptor 2 (TLR2), NEC exposed to the nasal carrier strain had a 4‐hr delay in TLR2 expression compared with NEC exposed to non‐carrierS. aureus. Moreover, even after 20 hr of colonization the expression of two principal epithelial antimicrobial peptides, human β‐defensin‐2 and human β‐defensin‐3, was negligibly induced in NEC exposed to the nasal carrier strain ofS. aureusin comparison to the non‐carrier strain. These results suggest that carrier strains ofS. aureusretain a competitive advantage over non‐carrier strains by delaying the host's innate response to epithelial colonization and infection.
