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dc.creatorSaksida, Tamara
dc.creatorKoprivica, Ivan
dc.creatorVujičić, Milica
dc.creatorStošić-Grujičić, Stanislava
dc.creatorPerović, Milka
dc.creatorKanazir, Selma
dc.creatorStojanović, Ivana
dc.date.accessioned2018-01-09T10:24:29Z
dc.date.available2900-01-01
dc.date.issued2018
dc.identifier.issn1387-2877
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/pubmed/29254086
dc.identifier.urihttps://ibiss-r.rcub.bg.ac.rs/handle/123456789/2948
dc.description.abstractAlzheimer's disease (AD) is characterized by accumulation of amyloid-β plaques that further promotes microglia-mediated neuroinflammatory responses and inflammation in the brain. Emerging data are revealing the relation between gut-associated lymphoid tissue (GALT) cells and CNS, as effector cells primed in the gut might home to the brain. This study aimed to determine cell composition of GALT in 5xFAD mice, an established model for AD. Immune cells isolated from Peyer's patches (PP) and mesenteric lymph nodes (MLN) were stained with surface and intracellular markers for T helper (Th) subpopulations, B lymphocytes and macrophages and analyzed cytofluorimetrically, while cytokine expression and production were determined by qPCR and ELISA, respectively. Inflammation was detected in GALT of 5xFAD mice with established AD pathology. Although the production of IFN-γ, IL-4, and IL-10 was comparable between the strains, lower IL-17 production was observed in PP and MLN cells. This phenomenon could not be attributed to a lower abundance of Th17 cells, or cytokines that initiate their formation or propagation (TGF-β, IL-6, and IL-23). Also, reduced IL-17 production was not a consequence of altered Il-17 mRNA transcription or deficiency of Rorγt, a key transcription factor for IL-17. However, the expression of miR-155 (a non-coding micro RNA that promotes the development of Th17 cells), was significantly lower in MLN cells of 5xFAD mice. In contrast, mice without AD neuropathology did not have inflammation in GALT or altered Th17 numbers, nor decreased IL-17 production. In conclusion, the observed changes in GALT of 5xFAD mice mirror the disease progression and might reflect inadequate immune surveillance in the gut and lead to enhanced AD pathology.
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173056/RS//
dc.relationinfo:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173013/RS//
dc.relationNational Institutes of Health (1R03AG046216)
dc.rightsrestrictedAccess
dc.sourceJournal of Alzheimer's disease : JAD
dc.sourceJournal of Alzheimer's disease : JAD
dc.subject5xFAD mice
dc.subjectIL-17
dc.subjectPeyer’s patches
dc.subjectAmyloid-β
dc.subjectMesenteric lymph nodes
dc.titleImpaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology
dc.typearticleen
dc.rights.licenseARR
dcterms.abstractСаксида, Тамара; Копривица, Иван; Перовић, Милка; Каназир, Селма; Стојановић, Ивана; Стошић-Грујичић, Станислава; Вујичић, Милица;
dc.rights.holder© 2018 - IOS Press and the authors.
dc.citation.issue2
dc.citation.volume61
dc.identifier.doi10.3233/JAD-170538
dc.identifier.pmid29254086
dc.identifier.scopus2-s2.0-85038865904
dc.identifier.wos000422844100015
dc.citation.apaSaksida, T., Koprivica, I., Vujičić, M., Stošić-Grujičić, S., Perović, M., Kanazir, S., & Stojanović, I. (2018). Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology. Journal of Alzheimer’s disease : JAD, 61(2), 619–630.
dc.citation.vancouverSaksida T, Koprivica I, Vujičić M, Stošić-Grujičić S, Perović M, Kanazir S, Stojanović I. Impaired IL-17 Production in Gut-Residing Immune Cells of 5xFAD Mice with Alzheimer’s Disease Pathology. J Alzheimers Dis. 2018;61(2):619–30.
dc.citation.spage619
dc.citation.epage630
dc.type.versionpublishedVersionen
dc.citation.rankM21


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