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Potential of the Flavonoid Apigenin in Regulating Immune Cell Functions
Start Date: 12/4/2018Start Time: 1:30 PM
End Date: 12/4/2018End Time: 3:30 PM

Event Description
BIOMED PhD Thesis Defense

Potential of the Flavonoid Apigenin in Regulating Immune Cell Functions During Neuroinflammation in a RelB-dependent Manner

Rashida Ginwala, PhD Candidate
School of Biomedical Engineering, Science and Health Systems
Drexel University

Pooja Jain, PhD
Professor of Microbiology and Immunology
Drexel University College of Medicine

Adrian Shieh, PhD
Associate Teaching Professor
School of Biomedical Engineering, Science and Health Systems
Drexel University

Apigenin, a well-documented health promoting agent, belongs to a group of low-molecular weight phyto-pigments called flavonoids that are present ubiquitously in a variety of plants, vegetables and herbs. The chemo-protective effects of apigenin can be largely attributed towards its anti-inflammatory properties that have been studied in various cell types including the cells of the immune system such as dendritic cells (DCs). DCs are the most potent antigen presenting cells that form an important link between the innate and adaptive branches of the immune system through their ability to capture and present both pathogens and self-antigens and initiate either an immunogenic or tolerogenic response. Any dysregulation in this function causes an immune imbalance, sometimes leading to chronic inflammation that has been reported to be intimately linked to the development or worsening of several non-infectious diseases. The existing therapies for most of these chronic conditions sometimes leave more debilitating effects than the disease itself, warranting the advent of safer, and more cost-effective therapeutic alternatives for the patients. These inflammatory conditions are especially devastating in an immune-privileged location like the central nervous system (CNS).

In order to establish the potential utility of apigenin as a therapeutic agent against neuroinflammatory diseases, we tested and found that apigenin treatment ameliorated disease severity, progression and relapse of experimental autoimmune encephalomyelitis (EAE) in SJL/J mouse models of multiple sclerosis (MS). An increased retention of DCs and other myeloid cells in the periphery correlated with decreased immune cell infiltration and reduced demyelination in the treated mice. At the cellular level, apigenin was seen to induce a regulatory phenotype in human total blood DCs through reduction in cell surface expression of antigen presentation molecules (MHC I and MHC II), and co-stimulatory markers (CD40, CD80, CD83, and CD86). We found that Apigenin possibly exerts its effects through shifting the DC modulated T-cell responses from Th1 and Th17 type towards Treg directed responses evident through the decrease in T-bet, IFN-γ (Th1), IL-17 (Th17) and increase IL-10, TGF-β and FoxP3 (Treg) expression.

Mechanistically, apigenin treatment reduced cytoplasmic RelB expression in presence of TLR4 ligand, LPS, in human peripheral blood DCs, which is central to DC maturation, its antigen presentation capabilities and DC-mediated T-cell activation. Apigenin also decreased the mRNA and protein levels of RelB downstream targets, TNF-α, CD40, and CD86 in these DCs. These RelB-mediated effects of apigenin were potentiated in the absence of RelB thus confirming its role in apigenin directed regulation of DC biology. These results provide key information about the molecular events controlled by apigenin in its regulation of DC activity marking its potential as a therapy for neuroinflammatory disease.
Contact Information:
Name: Ken Barbee
Phone: 215-895-1335
Email: barbee@drexel.edu
Rashida Ginwala
Queen Lane Campus, Student Activities Center (SAC) 'A', located at 2900 Queen Lane, Philadelphia, PA. A shuttle is available from 33rd and Market Streets.
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