Author/Authors :
Jamalidoust، Marzieh نويسنده Department of Virology, Professor Alborzi Clinical Microbiology Research Center, Nemazi Hospital, Shiraz University of Medical Sciences, Shiraz, IR Iran , , Ravanshad، Mehrdad نويسنده Department of Virology, Faculty of Medical Sciences, Department of Virology, Faculty of Medical Sciences, Tarb, P.O. Box 14115-331, Tehran, I.R. Iran , , Namayandeh، Mandana نويسنده Department of Medical Virology, Prof. Alborzi Clinical Microbiology Research Center, Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, IR Iran , , Zare، Maryam نويسنده Department of Community Health Nursing, School of Nursing and Midwifery, Shiraz University of Medical Sciences, Shiraz, Iran , , Asaei، Sadaf نويسنده Professor Alborzi Clinical Microbiology Research Center, Namazi Hospital, Shiraz University of Medical Sciences, Shiraz, IR Iran , , Ziyaeyan، Mazyar نويسنده ,
Abstract :
Interleukin-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. The 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. The 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. Aβ (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. It 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.
