Nicotinamide mononucleotide (NMN) alleviates the poly(I:C)-induced inflammatory response in human primary cell cultures

Nicotinamide mononucleotide (NMN) alleviates the poly(I:C)-induced inflammatory response in human primary cell cultures

NMN: A Potential Regulator for Alleviating Inflammation and Enhancing Mitochondrial Function

Introduction: NMN, or nicotinamide mononucleotide, is a direct precursor of NAD+ and has been found to play a crucial role in increasing NAD+ levels and mitochondrial activity in cells. Recent research has explored the potential anti-inflammatory properties of NMN and its implications in treating chronic or acute inflammation. This article summarizes the key findings and implications of a study that investigated how NMN can alleviate the inflammatory response induced by poly(I:C) in human primary cells.

NMN and Cellular Function:

NMN has shown positive effects on age-associated physical decline in mice, including improved energy metabolism and insulin sensitivity. Elevating cellular NAD+ levels through NMN supplementation enhances metabolic processes and acts as a cellular stress response. Moreover, NAD+ supplementation may protect the lungs from inflammatory injury caused by SARS-CoV-2 infection.

Poly(I:C) and Inflammatory Response:

Poly(I:C) is a synthetic analog of viral double-stranded RNA used to model the inflammatory response induced by viral infection. Activation of poly(I:C) triggers the production of inflammatory mediators, including IL6 and PARP family members. NMN supplementation has been shown to suppress proinflammatory cytokine production in activated macrophages, suggesting its potential in reducing inflammation.

Key Findings of the Study:

The study investigated the effects of NMN on the inflammatory response induced by poly(I:C) in human primary cells. Transcriptome analysis revealed that NMN treatment alleviated the increased expression of inflammatory response-related factors, including IL6 and PARP family members, under poly(I:C)-activated conditions. Weighted gene correlation network analysis and Bayesian network analysis identified common and distinct genes and pathways that regulate the inflammatory response.

Implications and Future Research:

The study suggests that NMN may have a regulatory mechanism for alleviating inflammatory pathway activation, making it a potential therapeutic intervention for diseases with inflammation, such as cardiovascular diseases and viral infections. Furthermore, the involvement of the platelet-derived growth factor (PDGF) pathway in the anti-inflammatory activity of NMN indicates its potential in resolving the cytokine storm triggered by viral infections. Additional experimental measures, including protein abundance and NAD+ levels, would provide further support for the findings of this study.

Supplementary Information and Data Access:

Supplementary information, including data files and tables, is available for further reference. The raw and processed RNA-seq data from the study can be accessed at the NCBI GEO database using the accession number GSE233679. Additionally, the codes used in the study for various analyses are available in a GitHub repository.

Conclusion:

NMN, as a precursor of NAD+, demonstrates potential as a regulator for alleviating inflammation and enhancing mitochondrial function. The study highlights the anti-inflammatory activity of NMN and its implications for various diseases associated with inflammation. Further research in this field could contribute to the development of novel therapeutic interventions targeting inflammatory pathways.

Title of paper: Nicotinamide mononucleotide (NMN) alleviates the poly(I:C)-induced inflammatory response in human primary cell cultures

Author(s): Sano H, Kratz A, Nishino T, Imamura H, Yoshida Y, Shimizu N, Kitano H, Yachie A.

Year published: 2023

Published in: Sci Rep

Original article can be found here.

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