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The Role of Secondary Metabolites in Inflammation

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (15 February 2023) | Viewed by 2499

Special Issue Editor

Ghent University, Ghent, Belgium
Interests: inflammation; immunity; signal transduction; molecular evolution; reporter systems; genetic models; abscisic acid; salicylic acid; indole-3-acetic acid; cytokinins

Special Issue Information

Dear Colleagues,

Secondary (or specialized) metabolites is a very broad term for a variety of small molecules that often have profound physiological effects. Common for many of these molecules is that they regulate inflammation, and often the interaction between primary metabolism and inflammation, but the exact mechanism is often poorly understood. Some secondary metabolites are well-known hormones, such as those originating from steroid biosynthesis (glucocorticoids, sex hormones, etc.) or from amino acid metabolism (serotonin, dopamine, etc.), and other well-known molecules, such as kyneurins and prostaglandins. Lesser-known secondary metabolites that are also endogenously generated are the classical plant hormones abscisic acid (ABA), cytokinins (CKs), indole-3-acetic acid (Auxin), and salicylic acid (SA). For many of these molecules, elucidating their roles is further complicated by the fact that they may originate from several different sources, such as endogenous biosynthesis, microbiota, or nutrition.

We warmly welcome submissions, including original papers and reviews, investigating the signaling effects from secondary metabolites and their effect on inflammation and inflammation-related diseases.

Dr. Jens Staal
Guest Editor

Manuscript Submission Information

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Keywords

  • inflammation
  • immunometabolism
  • specialized metabolism
  • secondary metabolites
  • small molecules
  • hormones
  • homeostasis

Published Papers (1 paper)

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Research

17 pages, 2506 KiB  
Article
Nitrate Utilization Promotes Systemic Infection of Salmonella Typhimurium in Mice
by Wanwu Li, Linxing Li, Xiaolin Yan, Pan Wu, Tianli Zhang, Yu Fan, Shuai Ma, Xinyue Wang and Lingyan Jiang
Int. J. Mol. Sci. 2022, 23(13), 7220; https://doi.org/10.3390/ijms23137220 - 29 Jun 2022
Cited by 7 | Viewed by 1878
Abstract
Salmonella Typhimurium is an invasive enteric pathogen that causes gastroenteritis in humans and life-threatening systemic infections in mice. During infection of the intestine, S. Typhimurium can exploit nitrate as an electron acceptor to enhance its growth. However, the roles of nitrate on S. [...] Read more.
Salmonella Typhimurium is an invasive enteric pathogen that causes gastroenteritis in humans and life-threatening systemic infections in mice. During infection of the intestine, S. Typhimurium can exploit nitrate as an electron acceptor to enhance its growth. However, the roles of nitrate on S. Typhimurium systemic infection are unknown. In this study, nitrate levels were found to be significantly increased in the liver and spleen of mice systemically infected by S. Typhimurium. Mutations in genes encoding nitrate transmembrane transporter (narK) or nitrate-producing flavohemoprotein (hmpA) decreased the replication of S. Typhimurium in macrophages and reduced systemic infection in vivo, suggesting that nitrate utilization promotes S. Typhimurium systemic virulence. Moreover, nitrate utilization contributes to the acidification of the S. Typhimurium cytoplasm, which can sustain the virulence of S. Typhimurium by increasing the transcription of virulence genes encoding on Salmonella pathogenicity island 2 (SPI-2). Furthermore, the growth advantage of S. Typhimurium conferred by nitrate utilization occurred only under low-oxygen conditions, and the nitrate utilization was activated by both the global regulator Fnr and the nitrate-sensing two-component system NarX-NarL. Collectively, this study revealed a novel mechanism adopted by Salmonella to interact with its host and increase its virulence. Full article
(This article belongs to the Special Issue The Role of Secondary Metabolites in Inflammation)
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