Development of an in vitro immunobiotic evaluation system against rotavirus infection in bovine intestinal epitheliocytes

• Published in: Beneficial microbes Vol. 8; no. 2; p. 309
• Main Authors: Kobayashi, H, Kanmani, P, Ishizuka, T, Miyazaki, A, Soma, J, Albarracin, L, Suda, Y, Nochi, T, Aso, H, Iwabuchi, N, Xiao, J-Z, Saito, T, Villena, J, Kitazawa, H
• Format: Journal Article
• Language: English
• Published: Netherlands 26-04-2017
• Subjects: Animals; Bifidobacterium; Cattle; Cell Line; Cytokines - biosynthesis; DEAD Box Protein 58 - immunology; Enzyme Activation - drug effects; Epithelial Cells - immunology; Epithelial Cells - virology; Immunity, Innate - immunology; Interferon Regulatory Factor-3 - metabolism; Interferon-beta - immunology; Intestinal Mucosa - cytology; Intestinal Mucosa - immunology; Intestinal Mucosa - virology; Probiotics - pharmacology; Rotavirus - immunology; Rotavirus Infections - immunology; Rotavirus Infections - therapy; Rotavirus Infections - virology; TNF Receptor-Associated Factor 3 - metabolism; Toll-Like Receptor 3 - immunology; immunoregulation; bifidobacteria; bovine intestinal epithelial cells; rotavirus; antiviral response; immunobiotics
• ISSN: 1876-2891
• DOI: 10.3920/BM2016.0155

The bovine intestinal epithelial cell line (BIE cells) expresses the Toll-like receptor (TLR)3 and is able to mount an antiviral immune response after the stimulation with poly(I:C). In the present study, we aimed to further characterise the antiviral defence mechanisms in BIE cells by evaluating the innate immune response triggered by rotavirus (RV) infection. In addition, we attempted to determine whether immunobiotic bifidobacteria are able to confer protection of BIE cells against RV infection by beneficially modulating the antiviral immune response. RV OSU (porcine) and UK (bovine) effectively infected BIE cells, while a significant lower capacity to infect BIE cells was observed for human (Wa) and murine (EW) RV. We observed that viral infection in BIE cells triggered TLR3/RIG-I-mediated immune responses with activation of IRF3 and TRAF3, induction of interferon beta (IFN-β) and up-regulation of inflammatory cytokines. Our results also demonstrated that preventive treatments with Bifidobacterium infantis MCC12 or Bifidobacterium breve MCC1274 significantly reduced RV titres in infected BIE cells and differentially modulated the innate immune response. Of note, both strains significantly improved the production of the antiviral factor IFN-β in RV-infected BIE cells. In conclusion, this work provides comprehensive information on the antiviral immune response of BIE cells against RV, that can be further studied for the development of strategies aimed to improve antiviral defences in bovine intestinal epithelial cells. Our results also demonstrate that BIE cells could be used as a newly immunobiotic evaluation system against RV infection for application in the bovine host.