ArticleJundishapur journal of microbiology2016
Construction of AAV-rat-IL4 and Evaluation of its Modulating Effect on Aβ (1-42)-Induced Proinflammatory Cytokines in Primary Microglia and the B92 Cell Line by Quantitative PCR Assay.
Article in Jundishapur journal of microbiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Immunomodulatory effects of platelet-rich plasma on inflammatory and metabolic responses of B92 glial cells exposed to heat-killed Escherichia coli.Molecular biology reports · 2026Article
- Dantrolene : From Malignant Hyperthermia to Alzheimer's Disease.CNS & neurological disorders drug targets · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterleukin-4 (IL-4), as the most prominent anti-inflammatory cytokine, plays an important role in modulating microglial activation and inflammatory responses in Alzheimer's disease (AD), a chronic inflammatory disorder.
objectivesThe current study aimed to develop a new recombinant Adeno-associated viral (rAAV) vector that delivers IL-4 and then assess the counterbalancing effect of the new construct along with recombinant IL-4 (rIL-4) protein in in-vitro models of AD. MATERIALS AND
methodsThe rAAV-IL4 was originally prepared and then employed along with rIL-4 protein to counter Amyloid β (1-42)-induced proinflammatory cytokines in a primary microglia cell culture and the B92 rat microglia continuous cell line, using relative Real-Time PCR assay.
resultsAβ (1-42) stimulated the production of the proinflammatory cytokines IL6, IL1β, TNFα, and IL18 in both the primary microglia cell culture and the B92 cell line. Both the rAAV-IL4 construct and the rIL-4 protein were found to inhibit production of the most important Aβ (1-42)-induced proinflammatory cytokine mRNAs in the two types of cells with different patterns.
conclusionsIt seems that the new construct can serve as an appropriate option in the modulation of Aβ-induced proinflammatory cytokine gene expression and microglia activation in patients affected by AD.
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