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dc.contributor.authorRamirez, Alejandor
dc.contributor.authorRathinam, Vijay A. K.
dc.contributor.authorFitzgerald, Katherine A.
dc.contributor.authorGolenbock, Douglas T.
dc.contributor.authorMathew, Anuja
dc.date2022-08-11T08:09:41.000
dc.date.accessioned2022-08-23T16:39:59Z
dc.date.available2022-08-23T16:39:59Z
dc.date.issued2012-12-11
dc.date.submitted2013-03-04
dc.identifier.citationImmun Ageing. 2012 Dec 11;9(1):27. doi: 10.1186/1742-4933-9-27. <a href="http://dx.doi.org/10.1186/1742-4933-9-27" target="_blank">Link to article on publisher's site</a> 2012 Ramirez et al.; licensee BioMed Central Ltd.
dc.identifier.issn1742-4933 (Linking)
dc.identifier.doi10.1186/1742-4933-9-27
dc.identifier.pmid23228123
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39589
dc.description.abstractBACKGROUND: Cytokines regulated by the inflammasome pathway have been extensively implicated in various age-related immune pathologies. We set out to elucidate the contribution of the nod-like receptor protein 3 (NLRP3) inflammasome pathway to the previously described deficiencies in IL-1beta production by macrophages from aged mice. We examined the production of pro-IL-1beta and its conversion into IL-1beta as two separate steps and compared these cytokine responses in bone marrow derived macrophages from young (6-8 weeks) and aged (18-24 months) C57BL/6 mice. FINDINGS: Relative to macrophages from young mice, macrophages from aged mice produced less pro-IL-1beta after TLR4 stimulation with LPS. However upon activation of the NLRP3 inflammasome with ATP, macrophages from young and aged mice were able to efficiently convert and secrete intracellular pro-cytokines as functional cytokines. CONCLUSIONS: Lower levels of IL-1beta production are a result of slower and lower overall production of pro-IL-1beta in macrophages from aged mice.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=23228123&dopt=Abstract">Link to Article in PubMed</a>
dc.rights© 2012 Ramirez et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.subjectInterleukin-1beta
dc.subjectMacrophages
dc.subjectCarrier Proteins
dc.subjectImmunology and Infectious Disease
dc.titleDefective pro-IL-1beta responses in macrophages from aged mice
dc.typeJournal Article
dc.source.journaltitleImmunity and ageing : I and A
dc.source.volume9
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3383&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2383
dc.identifier.contextkey3830683
refterms.dateFOA2022-08-23T16:39:59Z
html.description.abstract<p>BACKGROUND: Cytokines regulated by the inflammasome pathway have been extensively implicated in various age-related immune pathologies. We set out to elucidate the contribution of the nod-like receptor protein 3 (NLRP3) inflammasome pathway to the previously described deficiencies in IL-1beta production by macrophages from aged mice. We examined the production of pro-IL-1beta and its conversion into IL-1beta as two separate steps and compared these cytokine responses in bone marrow derived macrophages from young (6-8 weeks) and aged (18-24 months) C57BL/6 mice.</p> <p>FINDINGS: Relative to macrophages from young mice, macrophages from aged mice produced less pro-IL-1beta after TLR4 stimulation with LPS. However upon activation of the NLRP3 inflammasome with ATP, macrophages from young and aged mice were able to efficiently convert and secrete intracellular pro-cytokines as functional cytokines.</p> <p>CONCLUSIONS: Lower levels of IL-1beta production are a result of slower and lower overall production of pro-IL-1beta in macrophages from aged mice.</p>
dc.identifier.submissionpathoapubs/2383
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.source.pages27


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