ArticleMolecular nutrition & food research2022
Myo-Inositol in Fermented Sugar Matrix Improves Human Macrophage Function.
Article in Molecular nutrition & food research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- FBXO22 promotes hepatocellular carcinoma progression via paracrine myo‑inositol‑induced M2‑type polarization of macrophages.International journal of molecular medicine · 2026Article
- Yiqi Daozhi Formula Reduces the M1 Polarization of Macrophages in Mice With Postoperative Ileus Through Mediating Glycolysis Metabolism.Immunity, inflammation and disease · 2026Article
- Integrated omics identifies molecular networks of brain-body interactions of brain injury.iScience · 2025Article
- Primary Human M2 Macrophage Subtypes Are Distinguishable by Aqueous Metabolite Profiles.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
scopeReactive oxygen species production by innate immune cells plays a central role in host defense against invading pathogens at wound-site. A weakened host-defense results in persistent infection leading to wound chronicity. Fermented Papaya Preparation (FPP), a complex sugar matrix, bolsters respiratory burst activity and improves wound healing outcomes in chronic wound patients. The objective of the current study was to identify underlying molecular factor/s responsible for augmenting macrophage host defense mechanisms following FPP supplementation. METHODS AND
resultsIn depth LC-MS/MS analysis of cells supplemented with FPP led to identification of myo-inositol as a key determinant of FPP activity towards improving macrophage function. Myo-inositol, in quantities that is present in FPP, significantly improved macrophage respiratory burst and phagocytosis via de novo synthesis pathway of ISYNA1. In addition, myo-inositol transporters, HMIT and SMIT1, played a significant role in such activity. Blocking these pathways using siRNA attenuated FPP-induced improved macrophage host defense activities. FPP supplementation emerged as a novel approach to increase intracellular myo-inositol levels. Such supplementation also modified wound microenvironment in chronic wound patients to augment myo-inositol levels in wound fluid.
conclusionThese observations indicate that myo-inositol in FPP influences multiple aspects of macrophage function critical for host defense against invading pathogens.
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Registered trials
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