# miRNA-146b Targets TRAF6 and Inhibits LTA-Induced Inflammation of Bovine Mammary Epithelial Cells

## TL;DR

This study shows that miR-146b reduces inflammation in cow mammary cells by targeting TRAF6, suggesting it could help treat mastitis.

## Contribution

The study identifies miR-146b as a novel regulator of inflammation in bovine mammary epithelial cells through TRAF6 and NF-κB signaling.

## Key findings

- miR-146b targets TRAF6 and inhibits inflammation in bovine mammary epithelial cells.
- Overexpression of miR-146b reduces pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6.
- Knockdown of miR-146b abolishes its anti-inflammatory effects.

## Abstract

The aim of this study was to investigate the regulatory effect of miR-146b on lipoteichoic acid-induced inflammatory response in dairy cow mammary epithelial cells. Our results indicate that miR-146b targets TRAF6, inhibits inflammation in dairy cow mammary epithelial cells, and promotes their cell viability. miR-146b and its target gene TRAF6 play a certain role in mammary gland development in dairy cows, which is expected to become an effective target for the treatment of mastitis.

Mastitis is an inflammatory disease of mammary tissue that impairs milk production and quality, thereby seriously threatening the economic viability of dairy farms. miRNAs, such as miR-146b, are emerging as new candidates for anti-inflammatory therapy, and their activity modulation may provide a basis for controlling inflammation. However, the exact role and underlying mechanisms of miR-146b in bovine mastitis and associated inflammatory pathways in bovine mammary epithelial cells are still unclear. To clarify this, we established an in vitro model by stimulating MAC-T cells with Lipoteichoic acid and investigated the miR-146b-associated molecular pathways. The data from this study showed increased miR-146b expression after LTA stimulation. Then, the dual-luciferase reporter assay identified TRAF6 as a genuine target of miR-146b. Overexpression of miR-146b repressed the TRAF6 level and NF-κB pathway activation. Consequently, the production and secretion of major pro-inflammatory cytokines, including TNF-α, IL-1β, and IL-6, were significantly repressed, which could be indicative of inhibition of the inflammation in the cell model. Meanwhile, knockdown of miR-146b abolished such benefits. Based on these findings, it is reasonable to conclude that miR-146b mitigates LTA-induced inflammatory responses in bovine mammary epithelial cells by directly targeting TRAF6 and downstream NF-κB signaling. The present study identifies the functional role of miR-146b in the regulation of inflammation in MAC-T cells and highlights its potential as a target in mastitis intervention.