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dc.contributor.authorSmetannikova, M.en_US
dc.contributor.authorShishkina, L.en_US
dc.contributor.authorZhukov, V.en_US
dc.contributor.authorFankin, I.en_US
dc.contributor.authorSergeyev, A.en_US
dc.contributor.authorSkarnovich, M.en_US
dc.contributor.authorPyankov, O.en_US
dc.contributor.authorPetrischenko, V.en_US
dc.contributor.authorBondarenko, V.en_US
dc.contributor.authorSergeyev, A.en_US
dc.contributor.editorNikolai P Bochkoven_US
dc.date.accessioned2017-05-03T16:55:40Z
dc.date.available2017-05-03T16:55:40Z
dc.date.issued2007en_US
dc.date.modified2009-04-15T09:44:13Z
dc.identifier.issn08696047en_US
dc.identifier.urihttp://hdl.handle.net/10072/22149
dc.description.abstractThe results of the study showed that subcutaneous kenalog (Kn) lowered the resistance of mice to influenza virus (InV), as was seen by a decrease in 50% lethal dose and an increase in the degree of pulmonary tissue lesion, and the susceptibility of the lungs to InV, seen by the fact that 50% aerogenic infective dose (AID50) was significantly higher in the main group (Kn+InV) than in controls, which received Hanks solution subcutaneously (HS+InV). In vitro, 50% infective doses of InV for suspension of pulmonary and tracheal cells, characterizing their susceptibility to InV, were similar in Kn mice and controls. At the same time, lower resistance and higher degree of pulmonary inflammation noted in Kn mice after receiving a dose of InV that was much higher than an infecting one, was accompanied by the prevalence in the number as well as phagocyte and superoxide-producing activity of neutrophiles (Nph) over the same parameters for alveolar macrophages (AMph) as early as two days after receiving InV dose, vs. InV-infected controls. Evidently, one of the reasons for lower resistance to InV after Kn administration is significant disbalance between the functional activity of AMph and Nph populations. Ineffective AMph clearance of the lungs from InV and excessive number of recruited Nph and products of tissue disintegration may favor the development of respiratory failure and infectious-toxic shock, which leads to lower resistance in animals which receive Kn before InV infection.en_US
dc.description.peerreviewedYesen_US
dc.description.publicationstatusYesen_AU
dc.languageRussianen_US
dc.language.isoen_AU
dc.publisherIzdatel'stvo Meditsinaen_US
dc.publisher.placeRussian Federationen_US
dc.publisher.urihttp://www.ncbi.nlm.nih.gov/pubmed/17338373en_AU
dc.relation.ispartofstudentpublicationNen_AU
dc.relation.ispartofpagefrom3en_US
dc.relation.ispartofpageto8en_US
dc.relation.ispartofissue1en_US
dc.relation.ispartofjournalRossiiskaya Akademiya Meditsinskikh Nauk. Vestniken_US
dc.relation.ispartofvolume2007en_US
dc.rights.retentionYen_AU
dc.subject.fieldofresearchcode270304en_US
dc.titleTarget-cell susceptibility and lung phagocyte activity in mice with influenza virus resistance lowered by glucocorticoidal immunosuppressionen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Peer Reviewed (HERDC)en_US
dc.type.codeC - Journal Articlesen_US
gro.date.issued2007
gro.hasfulltextNo Full Text


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