Effects of Small Intestinal Submucosa (SIS) on the Murine Innate Immune Microenvironment Induced by Heat-Killed Staphylococcus aureus 英文参考文献.docVIP

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Effects of Small Intestinal Submucosa (SIS) on the Murine Innate Immune Microenvironment Induced by Heat-Killed Staphylococcus aureus 英文参考文献.doc

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Effects of Small Intestinal Submucosa (SIS) on the Murine Innate Immune Microenvironment Induced by Heat-Killed Staphylococcus aureus 英文参考文献

EffectsofSmallIntestinalSubmucosa(SIS)ontheMurine InnateImmuneMicroenvironmentInducedbyHeat- KilledStaphylococcusaureus RoshniRoyChowdhury*,YoussefAachoui*,SwapanK.Ghosh* DepartmentofBiology,IndianaStateUniversity,TerreHaute,Indiana,UnitedStatesofAmerica Abstract The useof biological scaffold materials for wound healingand tissue remodeling has profoundlyimpacted regenerative medicine and tissue engineering. The porcine-derived small intestinal submucosa (SIS) is a licensed bioscaffold material regularlyusedinwoundandtissuerepair,oftenincontaminatedsurgicalfields.Complicationsandfailuresduetoinfection of this biomaterial have therefore been a major concern and challenge. SIS can be colonized and infected by wound- associated bacteria, particularly Staphylococcus aureus. In order to address this concern and develop novel intervention strategies, the immune microenvironment orchestrated by the combined action of S. aureus and SIS should be critically evaluated. Since the outcome of tissue remodeling is largely controlled by the local immune microenvironment, we assessed the innate immune profile in terms of cytokine/chemokine microenvironment and inflammasome-responsive genes.BALB/cmicewereinjectedintra-peritoneallywithheat-killedS.aureusinthepresenceorabsenceofSIS.Analysesof cytokines, chemokines and microarray profiling of inflammasome-related genes were done using peritoneal lavages collected24hoursafterinjection.ResultsshowedthatunlikeSIS,theS.aureus-SISinteractomewascharacterizedbyaTh1- biasedimmuneprofilewithincreasedexpressionsofIFN-c,IL-12anddecreasedexpressionsofIL-4,IL-13,IL-33andIL-6. SuchmodulationoftheTh1/Th2axiscangreatlyfacilitategraftrejections.TheS.aureus-SISexposurealsoaugmentedthe expressionsofpro-inflammatorycytokineslikeIL-1b,Tnf-a,CD30L,EotaxinandFractalkine.Thisheightenedinflammatory response caused by S. aureus contamination could enormously affect the biocompatibility of SIS. However, the mRNA expressionsofmanyinflammasome-relatedgeneslikeNl