ArticleProteome science2023
Proteomics analysis of methionine enkephalin upregulated macrophages against infection by the influenza-A virus.
Article in Proteome science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Methionine enkephalin upregulates the immune function of RAW264.7 cells to inhibit the infection of Nelson Bay orthoreoviruses.Scientific reports · 2025Article
- Methionine enkephalin upregulates toll-like receptors in macrophages to suppress severe fever with thrombocytopenia syndrome virus infection.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Macrophages have a vital role in phagocytosis and antiviral effect against invading influenza viruses. Previously, we found that methionine enkephalin (MENK) inhibited influenza virus infection by upregulating the "antiviral state" of macrophages. To investigate the immunoregulatory mechanism of action of MENK on macrophages, we employed proteomic analysis to identify differentially expressed proteins (DEPs) between macrophages infected with the influenza-A virus and cells infected with the influenza-A virus after pretreatment with MENK. A total of 215 DEPs were identified: 164 proteins had upregulated expression and 51 proteins had downregulated expression. Proteomics analysis showed that DEPs were highly enriched in "cytokine-cytokine receptor interaction", "phagosome", and "complement and coagulation cascades pathway". Proteomics analysis revealed that MENK could be an immune modulator or prophylactic for the prevention and treatment of influenza. MENK promoted the polarization of M1 macrophages, activated inflammatory responses, and enhanced phagocytosis and killing function by upregulating opsonizing receptors.
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Registered trials
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