Lipoteichoic Acid Is Involved in the Ability of the Immunobiotic Strain CRL1506 to Modulate the Intestinal Antiviral Innate Immunity Triggered by TLR3 Activation.

Studies have demonstrated that lipoteichoic acid (LTA) is involved in the immunomodulatory properties of some immunobiotic lactobacilli. The aim of this work was to evaluate whether LTA contributes to the capacity of CRL1506 in modulating the intestinal innate antiviral immune response. A D-alanyl-lipoteichoic acid biosynthesis protein () knockout CRL1506 strain (Δ) was obtained, and its ability to modulate Toll-like receptor (TLR)-3-mediated immune response was evaluated in porcine intestinal epithelial (PIE) cells and in Balb/c mice. Wild-type (WT) CRL1506 ( WT) was used as positive control. The challenge of PIE cells with the TLR3 agonist poly(I:C) significantly increased interferon (IFN)-β, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 expressions. PIE cells pretreated with Δ or WT showed higher levels of IFN-β while only WT significantly reduced the expression of IL-6 and MCP-1 when compared with poly(I:C)-treated control cells. The oral administration of WT to mice prior the intraperitoneal injection of poly(I:C) significantly increased IFN-β and IL-10 and reduced intraepithelial lymphocytes (CD3NK1.1CD8αα) and pro-inflammatory mediators (TNF-α, IL-6, and IL-15) in the intestinal mucosa. Similar to the WT strain, Δ-treated mice showed enhanced levels of IFN-β after poly(I:C) challenge. However, treatment of mice with Δ was not able to increase IL-10 or reduce CD3NK1.1CD8αα cells, TNF-α, IL-6, or IL-15 in the intestine. These results indicate that LTA would be a key molecule in the anti-inflammatory effect induced by the CRL1506 strain in the context of TLR3-mediated inflammation.