Issue Cover (May 2019)

Front cover: Neuroinflammation is the hallmark of Japanese Encephalitis virus (JEV) infection. We previously reported NOTCH mediated modulation of inflammation in JEV infected microglial cells (Kumari et al. 2016). Several reports suggested that the NOTCH signalling pathway may cross‐talk with TLR signalling pathway to control inflammation (Hu et al. 2008, Zhang et al. 2012, Palaga et al. 2008). Upon binding of NOTCH ligand to the receptor, the NOTCH Intracellular Domain (NICD) is cleaved by the gamma‐secretase enzyme and transported to the nucleus to activate target genes. We, therefore, further verified if there is any cross‐talk between the NOTCH and TLR7 pathway. We checked the NICD level in JEV infected TLR7 Mo (vivo‐Morpholino) treated mice brain. Using IHC techniques, we checked NICD expression in JEV infected mice brain sections. As shown in Figure, JEV infection significantly upregulated NICD expression (red) in activated microglia, whereas, knockdown of TLR7 significantly reduced NICD expression. This study implicated the involvement of NOTCH‐TLR7 cross‐talk in JEV mediated inflammation in the mice brain. Image content:  Activated NOTCH expressions in JEV infected mice brain. Immunohistochemical staining of NICD (red) and activated microglia marker, IBA‐1, (green) in JEV infected brain sections. Nucleus stained with DAPI (blue). The panel represented single cell imaging (x60 with oil) of NICD expression in JEV infected mice.Read the full article ‘ Japanese Encephalitis Virus‐induced let‐7a/b interacted with the NOTCH‐TLR7 pathway in microglia and facilitated neuronal death via caspase activation ’ by S. Mukherjee, I. Akbar, B. Kumari, S. Vrati, A. Basu, A. Banerjee ( J. Neurochem . 2019, vol. 149 (4), pp. 518–534) on doi: 10.1111/jnc.14645