<p>The mineral content in drinking water is an emerging regulator of intestinal health. While certain mineral waters are generally considered beneficial, their health effects under enteric infection conditions remain unclear. Here we show that Mg<sup>2+</sup> in drinking water exacerbates inflammation caused by enteric pathogen <i>Salmonella</i> Typhimurium via two interlinked mechanisms: direct activation of its key bacterial competition machinery type VI secretion system (T6SS) and indirect amplification through inflammation-driven dysbiosis. Mg<sup>2+</sup> depletes beneficial <i>Akkermansia</i> and enriches <i>Bacteroides</i>, elevating pro-inflammatory bile acids and arginine that enhance T6SS-mediated competitive fitness. These effects vary with host health and water sources. Our findings support the use of low-mineral water for vulnerable groups during infection risk periods, establishing Mg<sup>2+</sup> in drinking water as a modifiable risk factor for infectious enteritis.</p>

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Mg2+ in drinking water boosts Salmonella infection risk by rewiring gut ecology and virulence

  • Tanghao Liu,
  • Tao Dong,
  • Ting Zhang,
  • Xiaohui Bai

摘要

The mineral content in drinking water is an emerging regulator of intestinal health. While certain mineral waters are generally considered beneficial, their health effects under enteric infection conditions remain unclear. Here we show that Mg2+ in drinking water exacerbates inflammation caused by enteric pathogen Salmonella Typhimurium via two interlinked mechanisms: direct activation of its key bacterial competition machinery type VI secretion system (T6SS) and indirect amplification through inflammation-driven dysbiosis. Mg2+ depletes beneficial Akkermansia and enriches Bacteroides, elevating pro-inflammatory bile acids and arginine that enhance T6SS-mediated competitive fitness. These effects vary with host health and water sources. Our findings support the use of low-mineral water for vulnerable groups during infection risk periods, establishing Mg2+ in drinking water as a modifiable risk factor for infectious enteritis.