Interleukin-1 receptor type I gene-deficient mice are less susceptible to Staphylococcus epidermidis biomaterial-associated infection than are wild-type mice
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作者:
Boelens, JJ
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
Boelens, JJ
van der Poll, T
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
van der Poll, T
Zaat, SAJ
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
Zaat, SAJ
Murk, JLAN
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
Murk, JLAN
Weening, JJ
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
Weening, JJ
Dankert, J
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机构:Leiden Univ, Med Ctr, Dept Pediat, NL-2300 RC Leiden, Netherlands
Elevated concentrations of interleukin-1 (IL-1) were found in tissue surrounding biomaterials infected with Staphylococcus epidermidis. To determine the role of IL-1 in biomaterial-associated infection (BAI), IL-1 receptor type I-deficient (IL-1R(-/-)) and wild-type mice received subcutaneous implants of silicon elastomer (SE) or polyvinylpyrrolidone-grafted SE (SEpvp), combined with an injection of 10(6) CFU of S. epidermidis or sterile saline. Neither mouse strain was susceptible to BAI around SE. IL-1R(-/-) mice with SEpvp implants had a no abscess formation and a reduced susceptibility to persistent S. epidermidis infection. The normal foreign body response, characterized by giant-cell formation and encapsulation, was delayed around SEpvp in wildtype mice but not in IL-1R(-/-) mice. This coincided with enhanced local IL-4 production in IL-1R(-/-) mice. These data suggest that inhibition of local IL-1 activity may be beneficial for the outcome of BAI.