# Siderophore-mediated zinc acquisition enhances enterobacterial colonization of the inflamed gut

## TL;DR

This study shows how a probiotic E. coli strain uses a molecule called yersiniabactin to acquire zinc, helping it survive in the inflamed gut.

## Contribution

The study reveals a novel zinc acquisition mechanism via yersiniabactin in E. coli Nissle 1917.

## Key findings

- Nissle uses yersiniabactin as a zincophore to grow in zinc-limited environments.
- Yersiniabactin's zinc binding increases with higher pH, influencing metal acquisition.
- This mechanism allows Nissle to tolerate calprotectin and thrive in the inflamed gut.

## Abstract

Zinc is an essential cofactor for bacterial metabolism, and many Enterobacteriaceae express the zinc transporters ZnuABC and ZupT to acquire this metal in the host. However, the probiotic bacterium Escherichia coli Nissle 1917 (or “Nissle”) exhibits appreciable growth in zinc-limited media even when these transporters are deleted. Here, we show that Nissle utilizes the siderophore yersiniabactin as a zincophore, enabling Nissle to grow in zinc-limited media, to tolerate calprotectin-mediated zinc sequestration, and to thrive in the inflamed gut. We also show that yersiniabactin’s affinity for iron or zinc changes in a pH-dependent manner, with increased relative zinc binding as the pH increases. Thus, our results indicate that siderophore metal affinity can be influenced by the local environment and reveal a mechanism of zinc acquisition available to commensal and pathogenic Enterobacteriaceae.

Zinc is an essential cofactor for bacterial metabolism. Here, the authors show that the probiotic bacterium Escherichia coli Nissle 1917 utilizes the siderophore yersiniabactin as a zincophore, allowing the microbe to grow in zinc-limited media and to thrive in the inflamed gut.