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免疫抑制宿主肺部炎症反应及肿瘤坏死因子介导机制 被引量:4

Lipopolysaccharide(LPS)inducedpulmonaryinflammatoryresponseandefectsofTNFinimmunocon┐promisedhost(ICH)
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摘要 目的研究免疫抑制宿主(ICH)肺部炎症反应及肿瘤坏死因子(TNF)介导机制。方法复制ICH动物模型。ICH活体肺经气管给予内毒素(LPS)刺激,刺激前及刺激后1,3,5,8,24小时行支气管肺泡灌洗(BAL)。结果发现LPS刺激后5小时支气管肺泡灌洗液(BALF)中细胞总数显著增加。肺泡巨噬细胞(PAM)和中性粒细胞(PMN)数量均增高,但PAM比例因PMN比例升高而降低。肺组织病理发现有急性肺泡炎症反应。BALF中有大量TNF释放。BALF中TNF水平的增高与PMN进入肺泡腔在动力学上基本平行。血清TNF无明显升高。在炎症发展过程中,BALF中TNF升高与PMN的内流增加相平行。结论提示TNF可能是介导PMN内流和炎症的细胞因子(CKs)之一。ICH过高的TNF释放会引起肺损伤。在受到LPS刺激后ICH系统性炎症免疫反应抑制而肺部炎症依然剧烈,反映了“腔室化”现象存在。 ObjectiveToinvestigatethelulmonaryinflammatoryresponseandTNF-mediatedefectsinICH.MethodsICHmodelsofguineapigswereinducedsucesfulybyreceivingdailyintraperitonealinjectionsofcyclophosphamide(15mg·kg-1·d-1)plusdailysubcutaneousinjectionofcortisoneacetate(100mg·kg-1·d-1)foratotalof7conseutivedays.Onthedayafterthefinaldoseofdrugs,guineapigswerechalengedintratrachealywithPLS(200μg/animal)andwerelavagedbeforeand1,3,5,8,24hoursafterchalenged,respectively,respectively.ResultsFivehoursafterLPSchalenged,totalcountsofbronchoalveolarfluid(BLAF)celsandtheproportionofPMNincreasedsignificangtly.accomthoughthecountsofbothPAMandPMNincreased,theproportionofPAMdecreasedgradulyaccompaniedbyincreaseoftheproportionofPMNs.HematoxylineosinstainedlungsectionsafterchalengedwithLPSshowedanacuteintraalveolarinflammatoryresponse.Afterintra-trachealinjectionofLPS,theTNFlev-elinBALFprogressivelyincreased.BoththeTNFlevelandPMNcountstartedtoincreaseat1houraf-terLPSchalengs,peakedat5hours.TheTNFlevelinserumdidnotincreasemarkedlyafterintratra-chealinjectionofLPS.Inthedevelopmentofaninflammatoryresponse,alargeamountofTNFwerere-leasedinBALF,thelevelofTNFinBALFwascloselymatchedtheinfluxofPMN.ConclusionsThedatasuggestedthatTNFwasoneofthecytokineswhichmediatedinfluxofPMNsandinflammation.HighlevelofTNFreleasedinBALFofICHcouldinducethelunginjury.Thesystemicinflammatoryre-sponseofICHwasinvolvingimmunosuppresedstateafterintratrachealinjectionofLPS,however,strongintraalveolarinflammatoryresponsestiloccured,whichreflectedthephenomenonof“compart-mentalization”ininflammatoryresponse.
出处 《中华结核和呼吸杂志》 CAS CSCD 北大核心 1996年第3期143-147,共5页 Chinese Journal of Tuberculosis and Respiratory Diseases
关键词 肿瘤坏死因子 免疫抑制性宿主 肺部炎症反应 TumornecrosisfactorImmunocompromisedhostInflammation
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