Salmonella Typhimurium reprograms macrophage metabolism via T3SS effector SopE2 to promote intracellular replication and virulence

Lingyan Jiang, Peisheng Wang, Xiaorui Song, Huan Zhang, Shuangshuang Ma, Jingting Wang, Wanwu Li, Runxia Lv, Xiaoqian Liu, Shuai Ma, Jiaqi Yan, Haiyan Zhou, Di Huang, Zhihui Cheng, Chen Yang, Lu Feng () and Lei Wang ()
Additional contact information
Lingyan Jiang: Nankai University
Peisheng Wang: Nankai University
Xiaorui Song: Nankai University
Huan Zhang: Nankai University
Shuangshuang Ma: Nankai University
Jingting Wang: Nankai University
Wanwu Li: Nankai University
Runxia Lv: Nankai University
Xiaoqian Liu: Nankai University
Shuai Ma: Nankai University
Jiaqi Yan: College of Life Sciences, Nankai University
Haiyan Zhou: CAS-Key Laboratory of Synthetic Biology, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences
Di Huang: Nankai University
Zhihui Cheng: Nankai University
Chen Yang: CAS-Key Laboratory of Synthetic Biology, CAS Center for Excellence in Molecular Plant Sciences, Shanghai Institute of Plant Physiology and Ecology, Chinese Academy of Sciences
Lu Feng: Nankai University
Lei Wang: Nankai University

Nature Communications, 2021, vol. 12, issue 1, 1-18

Abstract: Abstract Salmonella Typhimurium establishes systemic infection by replicating in host macrophages. Here we show that macrophages infected with S. Typhimurium exhibit upregulated glycolysis and decreased serine synthesis, leading to accumulation of glycolytic intermediates. The effects on serine synthesis are mediated by bacterial protein SopE2, a type III secretion system (T3SS) effector encoded in pathogenicity island SPI-1. The changes in host metabolism promote intracellular replication of S. Typhimurium via two mechanisms: decreased glucose levels lead to upregulated bacterial uptake of 2- and 3-phosphoglycerate and phosphoenolpyruvate (carbon sources), while increased pyruvate and lactate levels induce upregulation of another pathogenicity island, SPI-2, known to encode virulence factors. Pharmacological or genetic inhibition of host glycolysis, activation of host serine synthesis, or deletion of either the bacterial transport or signal sensor systems for those host glycolytic intermediates impairs S. Typhimurium replication or virulence.

Date: 2021
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DOI: 10.1038/s41467-021-21186-4

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