Establishment and characterization of a sustained delayed-type hypersensitivity model with arthritic manifestations in C57BL6J mice.docVIP

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Establishment and characterization of a sustained delayed-type hypersensitivity model with arthritic manifestations in C57BL6J mice.doc

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Establishment and characterization of a sustained delayed-type hypersensitivity model with arthritic manifestations in C57BL6J mice

Atkinsonetal.ArthritisResearchTherapy2012,14:R134 /content/14/3/R134 RESEARCH ARTICLE OpenAccess Establishmentandcharacterizationofasustained delayed-typehypersensitivitymodelwitharthritic manifestationsinC57BL/6Jmice SaraMAtkinson1,2,PernilleAUsher3,PeterHKvist3,HelleMarkholst1,ClausHaase1*andAnnelineNansen1* Abstract Introduction:Rheumatoidarthritis(RA)isachronicprogressive,inflammatoryanddestructiveautoimmune disease,characterisedbysynovialjointinflammationandboneerosion.Tobetterunderstandthepathophysiology andunderlyingimmunemechanismsofRAvariousmodelsofarthritishavebeendevelopedindifferentinbred strainsofmice.EstablishmentofarthritismodelswithcomponentsofadaptiveimmunityintheC57BL/6Jstrainof micehasbeendifficult,andsincemostgeneticallymodifiedmicearecommonlybredonthisbackground,thereis aneedtoexplorenewwaysofobtainingrobustmodelsofarthritisinthisstrain.Thisstudywasundertakento establishandcharacteriseanovelmurinemodelofarthritis,thedelayed-typehypersensitivity(DTH)-arthritismodel, andevaluatewhetherdiseasecanbetreatedwithcompoundscurrentlyusedinthetreatmentofRA. Methods:DTH-arthritiswasinducedbyelicitingaclassicalDTHreactioninonepawwithmethylatedbovine serumalbumin(mBSA),withthemodificationthatacocktailoftypeIIcollagenmonoclonalantibodieswas administeredbetweentheimmunisationandchallengesteps.Involvedcellsubsetsandinflammatorymediators wereanalysed,andtissuesectionsevaluatedhistopathologically.Diseasewastreatedprophylacticallyand therapeuticallywithcompoundsusedinthetreatmentofRA. Results:WedemonstratethatDTH-arthritiscouldbeinducedinC57BL/6micewithpawswellinglastingforat least28daysandthatdiseaseinductionwasdependentonCD4+ cells.Weshowthatmacrophagesand neutrophilswereheavilyinvolvedintheobservedpathologyandthataclearprofileofinflammatorymediators associatedwiththesecellsubsetswasinducedlocally.Inaddition,inflammatorymarkerswereobserved systemically.Furthermore,wedemonstratethatdiseasecouldbebothpreventedandtreated. Conclusions:OurfindingsindicatethatD