Antiviral Role of Surface Layer Protein A (SlpA) of Lactobacillus acidophilus

TL;DR

A protein from Lactobacillus acidophilus may help prevent norovirus replication by boosting antiviral genes in immune cells.

Contribution

SlpA from Lactobacillus acidophilus enhances antiviral gene expression in macrophages, potentially preventing norovirus replication.

Findings

SlpA-treated RAWS cells show enhanced antiviral activity against murine norovirus.

SlpA treatment increases expression of Iigp1 and Ifit1 genes in infected cells.

Abstract

Norovirus is associated with vomiting and diarrhea and, in severe cases, can result in death. Currently, there is no effective treatment or vaccine for this virus. Bilateral interactions have been reported between gut microbiota and viral infection. Our laboratory has been studying the Surface layer protein A (SlpA) of a human isolate of Lactobacillus acidophilus. Previously, we reported that SlpA induces a variety of antiviral genes in human dendritic cells, suggesting it may prevent viral replication. SlpA binds to its cognate receptor SIGNR3-expressed on limited dendritic cells. To achieve a homogenous expression of the gene, we modified murine macrophage RAW 264.7 (RAW) cells by transducing SIGNR3-expressing lentivirus, resulting in RAWS cells. These cells and wild-type RAW cells were pretreated with SlpA for one hour and infected with 1 MOI of murine norovirus (MNV). We report that RAWS cells, when treated with SlpA, enhance the antiviral program to prevent viral replication, as determined by quantitative real-time PCR and viral titer. RNA isolated from MNV-infected cells revealed an elevation in two critical antiviral genes, Iigp1 and Ifit1, in SlpA-treated RAWS cells, potentially preventing viral replication.

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