Abstract
After peripheral nerve injury, a process of axonal degradation, debris clearance, and subsequent regeneration is initiated by complex local signaling, called Wallerian degeneration (WD). This process is in part mediated by neuroglia as well as infiltrating inflammatory cells and regulated by inflammatory mediators such as cytokines, chemokines, and the activation of transcription factors also related to the inflammatory response. Part of this neuroimmune signaling is mediated by the innate immune system, including arachidonic acid (AA) derivatives such as prostaglandins and leukotrienes. The enzymes responsible for their production, cyclooxygenases and lipooxygenases, also participate in nerve degeneration and regeneration. The interactions between signals for nerve regeneration and neuroinflammation go all the way down to the molecular level. In this paper, we discuss the role that AA derivatives might play during WD and nerve regeneration, and the therapeutic possibilities that arise.
Highlights
Nerve injury can occur at any point along the length of a peripheral nerve as it courses from the root through the plexus and to the target organ
Irrespective of cause, there is a limited range of responses to peripheral nerve injury of which the most important is Wallerian degeneration (WD)
COX-2 expression is locally upregulated, but this phenomenon has been mainly linked to the pathogenesis of neuropathic pain [23, 24], COX-1 could participate in tissue remodeling during WD in the spinal cord [25]
Summary
Nerve injury can occur at any point along the length of a peripheral nerve as it courses from the root through the plexus and to the target organ. WD is a sequential pattern of axonal degeneration, myelin degradation, and supporting glial cell proliferation lasting 24–48 h During this complex process, various events take place, including blood-nerve barrier dysfunction, endoneural space reorganization [1], and most importantly for our purposes, the induction of an intense inflammatory response, constituted by inflammatory mediator release and production [2]. Various events take place, including blood-nerve barrier dysfunction, endoneural space reorganization [1], and most importantly for our purposes, the induction of an intense inflammatory response, constituted by inflammatory mediator release and production [2] Axonal degeneration initiates this response, activating SC and macrophages, that prolipherate and activate, clearing myelin debris and producing cytokines that perpetuate an inflammatory state. In this paper we will discuss the available evidence that sheds light in this issue
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