ArticleMedComm2025
IL-37 Mitigates the Inflammatory Response in Macrophages Induced by SARS-CoV-2 Omicron Infection Through the NF-κB Signaling Pathway.
Article in MedComm, 2025. 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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Who cites it
4 citing papers in PubMed.
- Research progress on the role of IL‑37 in gynecological and obstetrics‑related diseases (Review).International journal of molecular medicine · 2026Review
- IL-37 and IL-36 Cytokine Profiles in Chronic Hepatitis Delta During Bulevirtide Therapy.Pathogens (Basel, Switzerland) · 2026Article
- Programmed Probiotics Generate Interleukin-37b-Bearing Nanovesicles In Situ for Precision Immunomodulation in Colitis.Research (Washington, D.C.) · 2026Article
- Interleukin-37 in respiratory diseases: molecular mechanisms and immune modulation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression levels of macrophage-associated cytokines are significantly greater in COVID-19 patients than in healthy individuals. Exploring strategies to modulate pathological cytokine storms can effectively prevent the development of severe coronavirus infection-induced pneumonia. Treatment with interleukin-37 (IL-37), an anti-inflammatory factor, has unique anti-inflammatory and antiviral effects on infections caused by various pathogens. In this study, we investigated the effect of IL-37 treatment on the SARS-CoV-2 Omicron-infection induced inflammatory response and its molecular mechanism. Our results demonstrated that IL-37 treatment effectively alleviated symptoms, reduced viral loads, suppressed the production of proinflammatory cytokines and chemokines both systemically (in serum) and locally (in the lungs), and attenuated lung lesions and inflammatory cell infiltration in Omicron-infected mice. The suppressed proinflammatory factors were macrophage-related, particularly CCL3 and CCL4, which were significantly inhibited. Furthermore, treatment with IL-37 significantly reduced the proportion of M1-type macrophages in lungs of Omicron-infected mice. In addition, we found that IL-37 targeted M1 macrophages through modulation of the NF-κB signaling pathway to suppress the production of proinflammtory factors during Omicron infection. This study elucidated the anti-inflammatory effect of IL-37 treatment on the Omicron-induced inflammatory response while identifying its specific target site, thereby providing fundamental insights for exploring potential clinical therapeutic interventions.
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