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dc.contributor.authorLim, Jae Hyang
dc.contributor.authorDavis, Roger J.
dc.contributor.authorLi, Jian-Dong
dc.date2022-08-11T08:08:16.000
dc.date.accessioned2022-08-23T15:49:01Z
dc.date.available2022-08-23T15:49:01Z
dc.date.issued2007-08-01
dc.date.submitted2016-05-25
dc.identifier.citationImmunity. 2007 Aug;27(2):349-60. <a href="http://dx.doi.org/10.1016/j.immuni.2007.07.011">Link to article on publisher's site</a>
dc.identifier.issn1074-7613 (Linking)
dc.identifier.doi10.1016/j.immuni.2007.07.011
dc.identifier.pmid17723219
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28334
dc.description<p>Full author list omitted for brevity. For full list of authors see article.</p>
dc.description.abstractStreptococcus pneumoniae (S. pneumoniae) causes high early mortality in pneumococcal pneumonia, which is characterized by acute lung injury (ALI). The molecular mechanisms underlying ALI and the high early mortality remain unknown. Despite recent studies that identify deubiquitinating enzyme cylindromatosis (CYLD) as a key regulator for T cell development, tumor cell proliferation, and NF-kappaB transcription factor signaling, its role in regulating bacteria-induced lethality, however, is unknown. Here, we showed that CYLD deficiency protected mice from S. pneumoniae pneumolysin (PLY)-induced ALI and lethality. CYLD was highly induced by PLY, and it inhibited MKK3-p38 kinase-dependent expression of plasminogen activator inhibitor-1 (PAI-1) in lung, thereby potentiating ALI and mortality. Thus, CYLD is detrimental for host survival, thereby indicating a mechanism underlying the high early mortality of pneumococcal pneumonia.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17723219&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/j.immuni.2007.07.011
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectImmunology of Infectious Disease
dc.subjectMolecular Biology
dc.titleTumor suppressor CYLD regulates acute lung injury in lethal Streptococcus pneumoniae infections
dc.typeJournal Article
dc.source.journaltitleImmunity
dc.source.volume27
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/60
dc.identifier.contextkey8646689
html.description.abstract<p>Streptococcus pneumoniae (S. pneumoniae) causes high early mortality in pneumococcal pneumonia, which is characterized by acute lung injury (ALI). The molecular mechanisms underlying ALI and the high early mortality remain unknown. Despite recent studies that identify deubiquitinating enzyme cylindromatosis (CYLD) as a key regulator for T cell development, tumor cell proliferation, and NF-kappaB transcription factor signaling, its role in regulating bacteria-induced lethality, however, is unknown. Here, we showed that CYLD deficiency protected mice from S. pneumoniae pneumolysin (PLY)-induced ALI and lethality. CYLD was highly induced by PLY, and it inhibited MKK3-p38 kinase-dependent expression of plasminogen activator inhibitor-1 (PAI-1) in lung, thereby potentiating ALI and mortality. Thus, CYLD is detrimental for host survival, thereby indicating a mechanism underlying the high early mortality of pneumococcal pneumonia.</p>
dc.identifier.submissionpathdavis/60
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages349-60


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