Abstract
In this work, we aimed to characterize the antiviral response of an originally established porcine intestinal epithelial cell line (PIE cells) by evaluating the molecular innate immune response to rotavirus (RVs). In addition, we aimed to select immunomodulatory bacteria with antiviral capabilities. PIE cells were inoculated with RVs isolated from different host species and the infective titers and the molecular innate immune response were evaluated. In addition, the protection against RVs infection and the modulation of immune response by different lactic acid bacteria (LAB) strains was studied. The RVs strains OSU (porcine) and UK (bovine) effectively infected PIE cells. Our results also showed that RVs infection in PIE cells triggered TLR3-, RIG-I- and MDA-5-mediated immune responses with activation of IRF3 and NF-κB, induction of IFN-β and up-regulation of the interferon stimulated genes MxA and RNase L. Among the LAB strains tested, Bifidobacterium infantis MCC12 and B. breve MCC1274 significantly reduced RVs titers in infected PIE cells. The beneficial effects of both bifidobacteria were associated with reduction of A20 expression, and improvements of IRF-3 activation, IFN-β production, and MxA and RNase L expressions. These results indicate the value of PIE cells for studying RVs molecular innate immune response in pigs and for the selection of beneficial bacteria with antiviral capabilities.
Highlights
Rotavirus (RVs) genome is constituted by 11-segmented double strand RNA encoding structural and non-structural proteins that allow virus to effectively infect intestinal epithelial cells (IECs) [1]
We evaluated the response of PIE cells to poly(I:C) challenge and found that monocyte chemotactic protein 1 (MCP-1), interleukin (IL)-8, tumor necrosis factor (TNF)-α, IL-6 and both IFN-α and IFN-β were up-regulated in PIE cells after stimulation indicating that PIE cells are a good tool to study in vitro the immune responses triggered by TLR3 on IECs
We demonstrated previously that bifidobacteria strains with a high capacity to stimulate TLR2 such as B. longum BB536 and B. breve M-16V were able to increase the expression of A20 in PIE cells and reduce TLR4-mediated inflammatory response [19, 44]
Summary
Rotavirus (RVs) genome is constituted by 11-segmented double strand RNA (dsRNA) encoding structural and non-structural proteins that allow virus to effectively infect intestinal epithelial cells (IECs) [1]. The innate immune response is critical for limiting RVs replication and disease in the host [6] In this regard, IECs have a crucial role in the defense against RVs through their capacity to express pattern recognition receptors (PRRs) able to sense viral molecules. Toll-like receptor (TLR)-3 is able to recognize dsRNA of RVs, leading to the activation of interferon (IFN) regulatory factors (IRFs) and nuclear factor (NF)-κB [1, 7]. Both IRFs (IRF3 and IFR7) and NF-κB are able to induce the production of INFs, especially type-I IFNs [8]. IFN-α and IFN-β play important roles in controlling RVs infection since the secretion of type I IFN results in the expression of several hundred IFN stimulated gene (ISG) products with antiviral activities, both within infected cells as well as in bystander cell populations [8]
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