Lack of effects of Resolvin D1 after spinal cord injury in mice

Abstract

Inflammation is a fundamental component of the body's response to injury or infection and is responsible for restoring tissue homeostasis and starting the wound healing process. To avoid excessive tissue damage, it is important to efficiently resolve inflammation once it is no longer necessary. In recent years, the discovery of pro-resolving lipid mediators derived from polyunsaturated fatty acids, such as Resolvin D1 (RvD1), has shed light on the resolution of inflammation. However, the impact of RvD1 on Spinal Cord Injury (SCI) remains unexplored. In this study, we provide direct evidence that the administration of RvD1 for one week after SCI fails to enhance resolution of inflammation and does not improve functional and histological outcomes. Our transcriptomic analysis reveals that RvD1 does not modulate inflammatory response pathways in the injured spinal cord but leads to significant changes in the expression of genes related to ribosomal function and extracellular matrix pathways. Unlike SCI, RvD1 treatment ameliorated neurological deficits in experimental autoimmune encephalomyelitis. Our findings represent the first report demonstrating that RvD1 treatment does not exert therapeutic actions in the context of SCI and suggest that this pro-resolving agonist may exert therapeutic actions in certain but not in all conditions involving an inflammatory component.