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Data on sulforaphane treatment mediated suppression of autoreactive, inflammatory M1 macrophages
Sanjima Pal1, V Badireenath Konkimalla1
1School of Biological Sciences, National Institute of Science Education and Research (NISER), PO Bhimpur-Padanpur, Via-Jatni, Khurda 752050, India.
Abstract:
Any chronic, inflammatory, autoimmune disease (e.g. arthritis) associated pathogenesis directs uncontrolled accumulation of both soluble forms of collagens in the synovial fluids and M1 macrophages around inflamed tissues. Despite of few studies demonstrating efficiency of Sulforaphane (SFN) in suppressing arthritis associated collagen restricted T cells or fibroblasts, its effects on macrophage polarity and plasticity are less understood. Recently, we reported regulation of phenotypic and functional switching by SFN in induced and spontaneously differentiating human monocytes [1]. Here, flow cytometry, western blot and ELISA derived data demonstrated that SFN inhibited in vitro inflammatory responses developed by soluble human collagens (I-IV) induced auto-reactive M1 type monocyte/macrophage model.
Insights
Sulforaphane (SFN) effectively suppresses inflammation in a model of autoimmune disease by inhibiting M1 macrophages. This study clarifies SFN
Area of Science:
- Immunology
- Rheumatology
- Molecular Biology
Background:
- Chronic inflammatory autoimmune diseases like arthritis involve collagen accumulation and M1 macrophage activation.
- Sulforaphane (SFN) shows potential in arthritis but its impact on macrophage plasticity is unclear.
Purpose of the Study:
- To investigate the effects of SFN on macrophage polarity and inflammatory responses.
- To determine if SFN can inhibit collagen-induced M1 macrophage activation.
Main Methods:
- Utilized flow cytometry, western blot, and ELISA.
- Developed an in vitro model using soluble human collagens (I-IV) to induce auto-reactive M1 macrophages.
Main Results:
- SFN demonstrated inhibition of inflammatory responses in the M1 macrophage model.
- Data confirmed SFN's role in modulating macrophage behavior.
Conclusions:
- SFN can suppress inflammatory responses driven by collagen in an M1 macrophage model.
- SFN represents a potential therapeutic agent for autoimmune inflammatory conditions.
