# Beta-2-Microglobulin Regulates Sheep Susceptibility to Escherichia coli F17b in Intestinal Epithelial Cells

## TL;DR

This study shows that Beta-2-microglobulin helps protect sheep intestinal cells from E. coli F17b by reducing bacterial adhesion and improving cell function.

## Contribution

The study reveals a new role of Beta-2-microglobulin in protecting sheep intestinal cells from E. coli F17b infection.

## Key findings

- Beta-2-microglobulin overexpression reduced E. coli F17b adhesion and improved cell proliferation and migration.
- Knocking down Beta-2-microglobulin increased bacterial adhesion and impaired cell function.
- Beta-2-microglobulin strengthens the intestinal epithelial barrier against E. coli F17b.

## Abstract

This study investigated how Beta-2-microglobulin affects sheep susceptibility to Escherichia coli F17b infections in intestinal epithelial cells. The main goal was to determine whether Beta-2-microglobulin influences bacterial adhesion and the function of intestinal epithelial cells. Results showed that Beta-2-microglobulin overexpression reduced Escherichia coli F17b adhesion and promoted intestinal epithelial cells proliferation and migration, while Beta-2-microglobulin knockdown increased adhesion and impaired cell function. The study concludes that Beta-2-microglobulin protects sheep intestinal epithelial cells by strengthening the epithelial barrier, offering insights for a potential breeding disease-resistant sheep and improving livestock health, thereby reducing economic losses in animal farming.

Beta-2-microglobulin (B2M) is a key component protein in the processing and presentation of major histocompatibility complex (MHC)-I antigens and plays an important role in the immune system regulation. Previous studies have shown that B2M is significantly overexpressed in the intestinal tissues of sheep that are resistant to E. coli F17b infection (defined by milder clinical symptoms post-challenge) compared to those that are susceptible (exhibiting severe diarrhea). Based on this finding, this study aimed to investigate whether B2M influences the adhesion of E. coli F17b to sheep intestinal epithelial cells (IECs) and to assess its role in regulating IEC proliferation and migration. We tested this by overexpressing and knocking down B2M in IECs, and then measured bacterial adhesion through colony counts and fimbrial gene expression (RT-qPCR). Moreover, cell health was assessed using proliferation (CCK-8 and EdU) and migration (scratch) assays. The results showed that upregulation of B2M expression inhibited E. coli F17b adhesion and promoted IEC proliferation and migration. Silencing B2M increased bacterial adhesion and impaired cell function. In summary, B2M helps protect sheep IECs from E. coli F17b by strengthening the epithelial barrier through improved cell growth, proliferation, and migration. These findings elucidate part of the host defense mechanism against E. coli F17b, providing a basis for further research.