We study infectious diseases, immune responses against infectious agents, vaccines and anti-microbial compounds. The main research projects are as follows:
- Congenital cytomegalovirus (CMV) infection occurs in 0.3% of all births, and causes birth defects and developmental abnormalities. Since saliva/urine of siblings is the major source of infection, it is essential to develop vaccines to protect pregnant women from infection. Using the guinea pig model, we scrutinize pathogenesis in the placenta and fetuses for vaccine development. We also screen and analyze novel anti-CMV compounds.
- Development of oral vaccines based on Lactococcus by using small animal models.
- Ulcerative colitis (UC) is an inflammatory bowel disease with an unknown etiology. We study the colonic flora related to the onset of UC in a dextran sulfate sodium (DSS)-induced mouse UC model, screen therapeutics in the model, and analyze their functional mechanisms.
- Innate immunity is the first line of host defense against microbial infection. Toll-like receptors (TLRs), a family of innate immune receptors, recognize pathogen-associated molecular patterns on infected microbes, and initiate inflammatory responses to prevent or eliminate infection. Whereas the inflammatory reaction is important against infection, it may sometimes cause tissue injury and inflammatory diseases, indicating that the activation of TLR signaling should be regulated adequately. In addition, we analyze various chemical compounds that modulate TLR signaling pathways and their regulatory mechanisms.
- Pathobiological studies on microbial infection and vaccine development
- Screening of novel antiviral compounds and analyses of their targeting processes
- Pathophysiological and therapeutic studies on mucosal infectious and inflammatory diseases in the gut
- Studies on the regulation/modulation of innate immune signaling
- Yamada S, Katano H, Sato Y, Fukuchi S, Hashimoto K, Inoue N, An ex vivo culture model for placental cytomegalovirus infection using slices of guinea pig placental tissue, Placenta 37, 85-88 (2016).
- aniguchi R, Koyano S, Suzutani T, Goishi K, Ito Y, Morioka I, Nakamura H, Yamada H, Oka A, Inoue N, A Thr72Ala polymorphism in the NKG2D gene is associated with early symptomatic congenital cytomegalovirus disease, Infection 43, 353-359 (2015).
- Atarashi K, Tanoue T, Ando M, Kamada N, Nagano Y, Narushima S, Suda W, Imaoka A, Setoyama H, Nagamori T, Ishikawa E, Shima T, Hara T, Kado S, Jinnohara T, Ohno H, Kondo T, Toyooka K, Watanabe E, Yokoyama S, Tokoro S, Mori H, Noguchi Y, Morita H, Ivanov II, Sugiyama T, et al. Th17 cell induction by adhesion of microbes to intestinal epithelial cells, Cell 163, 367-80 (2015).
- Yamada S, Fukuchi S, Hashimoto K, Fukui Y, Tsuda M, Kataoka M, Katano H, Inoue N, Guinea pig cytomegalovirus GP129/131/133, homologs of human cytomegalovirus UL128/130/131A, are required for viral entry into monocytes and macrophages, J. Gen. Virol., 95, 1376-1382 (2014).
- Sugiyama T, Takahashi K, Kuzumaki A, Tokoro S, Neri P, Mori H, Inhibitory mechanism of 10- hydroxy-trans-2-decenoic acid (royal jelly acid) against lipopolysaccharide- and interferon-β-induced nitric oxide production, Inflammation, 36, 372-378 (2013).