Resolvin D1 in the Lipopolysaccharide-Induced Inflammatory Microenvironment Mediates Resolution in Human Monocytic...

Area of Science:

• Immunology
• Molecular Biology

Background:

• Infectious triggers initiate systemic inflammation via immune cell activation and mediator release.
• Local mediators like resolvin D1 (RvD1) are crucial for resolving inflammation by interacting with immune cells.

Purpose of the Study:

• To investigate the impact of RvD1 on lipopolysaccharide (LPS)-induced inflammatory responses in monocytes.
• To elucidate the molecular mechanisms underlying RvD1's effect on monocyte-mediated inflammation.

Main Methods:

• Human THP-1 monocytic cells were treated with LPS and RvD1.
• Inflammatory cytokines (IL-1β, TNF-α) were quantified using ELISA.
• Gene expression and signaling pathways (NF-κB, MAPK p38) were analyzed via RNA-seq, RT-qPCR, and Western blotting.

Main Results:

• RvD1 significantly reduced IL-1β and TNF-α levels in LPS-induced inflammation.
• RvD1 modulated the expression of key genes including CREB, NRF2, BCL-2, and CASP3.
• RvD1 regulated NF-κB p65 and p38 MAPK signaling pathways, suppressing apoptotic factors.

Conclusions:

• RvD1 exhibits pro-resolving effects in monocyte inflammation.
• RvD1 regulates inflammation by modulating anti-apoptotic gene BCL-2 expression.
• RvD1 activates NF-κB p65 and MAPK p38 signaling pathways to resolve inflammation.