1. Academic Validation
  2. Monosodium Glutamate Inhibits Pseudomonas aeruginosa-Induced Acute Lung Injury by Targeting the Type III Secretion Systems and Modulating Host Immunity

Monosodium Glutamate Inhibits Pseudomonas aeruginosa-Induced Acute Lung Injury by Targeting the Type III Secretion Systems and Modulating Host Immunity

  • Microorganisms. 2026 Mar 23;14(3):725. doi: 10.3390/microorganisms14030725.
Jing Xu 1 2 Weiwei Wang 1 2 Yaxin Zhou 1 2 Hongxing Zhang 1 2 Zixuan Shang 1 2 Zhijin Zhang 1 2 Bing Li 1 2 Yubin Bai 1 2 Jiyu Zhang 1 2
Affiliations

Affiliations

  • 1 Key Laboratory of New Animal Drug Project of Gansu Province, Key Laboratory of Veterinary Pharmaceutical Development of the Ministry of Agriculture and Rural Affairs, Lanzhou Institute of Husbandry and Pharmaceutical Sciences, Chinese Academy of Agricultural Sciences, Lanzhou 730050, China.
  • 2 New Veterinary Drugs in Gansu Province Engineering Research Center, Key Laboratory of New Veterinary Drugs Engineering, Laboratory Animal Science Data Center of Gansu Province, Lanzhou Institute of Husbandry and Pharmaceutical Sciences, Chinese Academy of Agricultural Sciences, Lanzhou 730050, China.
Abstract

The opportunistic pathogen Pseudomonas aeruginosa poses a serious threat to immunocompromised patients. Monosodium glutamate (MSG), a widely used flavor enhancer, has been reported to possess anti-inflammatory and antioxidant properties. However, its therapeutic potential and mechanism against Pseudomonas aeruginosa (P. aeruginosa) Infection have remained unexplored. This study systematically elucidated the protective effects and molecular mechanisms of MSG against P. aeruginosa-induced acute lung injury (ALI). In a murine pneumonia model, MSG administration effectively alleviated lung pathological damage, edema, and inflammatory responses. Mechanistically, MSG exerted protection through a multifaceted strategy, including direct suppression of Bacterial virulence via binding to PopB of T3SS inhibition of the TLR4/MyD88/MAPK-driven inflammatory cascade and pro-inflammatory cytokine production, enhancement of endogenous antioxidant defense (SOD, CAT), and reshaping of pulmonary macrophages from the M1 to M2 phenotype. Notably, the anti-virulence effect of MSG, achieved by binding to PopB (KD = 3.52 × 10-6 M), presented a distinct advantage over traditional antimicrobials by potentially mitigating resistance development. Collectively, these findings indicated that MSG can alleviate ALI caused by P. aeruginosa Infection.

Keywords

PopB; acute lung injury; monosodium glutamate; type III secretion systems.

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