TheexpressionofIL-4inaratmodelofchronicpulmonaryinfectionbiofilmformationinducedbyPseudomonasaeruginosawasinvestigated,inwhichSPFWisterratswereinfectedviatracheawith0.1mlP.aeruginosastrainPAO579(10~9CFU/ml)inalginatebeadsortheplanktonicformofthisbacterialstrain(10~9CFU/ml),andon3,7and14dafterinfection,thebacteriologicalandpathologicalchangeswereobservedaswellastheexpressionofthecytokineIL-4wasdetermined.ItwasdemonstratedthatthecountofCFUperlungtissueincaseofbacteriainalginatebeadswassignificantlyhigherthanthatofbacteriainplanktonicform,withmoreseveregrosspathologicchangesandinflammatoryreactionsinthealginatebeadgroupincomparisonwiththatoftheplanktonicforms(P=0.002,P=0.004andP=0.002,respectively).Inaddition,theexpressionofIL-4inthealginatebeadgroupwasalsohigherthanthatintheplanktonicform(P=0.02,P=0.02andP=0.022,respectively).Apositivecorre-lationbetweenthelevelofIL-4expressionandthegrosslungpathologyinalginatebeadgroupexistedasdemonstratedbysimpleregressionanalysis(r=0.78,P<0.02).Itisconcludedthatthechronicpul-monaryinfectionwithbiofilmformationinducedbyP.aeruginosatendstohavetheprioritytotheTh2immuneresponse.
