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. 2018 Mar 2;9:326. doi: 10.3389/fimmu.2018.00326

Figure 2.

Figure 2

Beneficial effects of immunobiotics on the antiviral innate immune response against rotavirus in bovine intestinal epithelial (BIE) cells. Rotavirus doublestranded genomic RNA activates toll-like receptor 3 (TLR3), retinoic acid inducible gene-I (RIG-I), and melanoma differentiation-associated gene-5 (MDA-5), which are pattern recognition receptors (PRRs) expressed in IECs. Cellular signaling cascades mediated by interferon (IFN) regulatory factor-3 (IRF3) upregulate the expression of type I (IFN-α, IFN-β), and type III (IFNλ1, IFNλ2/3) IFN, which in turn induces the synthesis of IFN-stimulated genes with antiviral activities including: myxovirus resistance 1 IFN-inducible protein (Mx1), MxA, ribonuclease L (RNaseL), 2′-5′-oligoadenylate synthetase (OAS), and protein kinase R (PKR). Antiviral PRRs also activate nuclear factor κB (NF-κB) pathway and induce the secretion of proinflammatory cytokines and chemokines including: interleukin 6 (IL-6), IL-8, monocyte chemotactic protein 1 (MCP-1/CCL2), and IFN gamma-induced protein 10 (IP-10/CXCL10). Preventive treatment of BIE cells with immunobiotics increase the activation of IRF3, improve the production of the antiviral factors and differentially regulate the expression of inflammatory mediators.