Eicosanoids and Regulators
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About Eicosanoids and Regulators
Eicosanoids are a diverse group of lipid mediators derived from polyunsaturated fatty acids, particularly arachidonic acid. They play essential roles as local signaling molecules in various physiological and pathological processes, including inflammation, immune response, blood clotting, and vascular homeostasis. Eicosanoids are involved in regulating inflammation by modulating vascular permeability, vasodilation or vasoconstriction, and recruitment of immune cells.
There are three major classes of eicosanoids:
- Prostaglandins (PGs): Prostaglandins are the most well-known and widely studied group of eicosanoids. They are involved in a range of physiological functions, including inflammation. Prostaglandins regulate vasodilation, vascular permeability, and the recruitment of immune cells to the site of inflammation. Some prostaglandins, such as PGE2, can promote inflammation, while others, such as PGD2, have anti-inflammatory effects.
- Leukotrienes (LTs): Leukotrienes are potent lipid mediators primarily synthesized by immune cells, such as leukocytes and mast cells. They play a crucial role in allergic and inflammatory responses, particularly in bronchoconstriction, increased vascular permeability, and recruitment of immune cells. Leukotrienes, such as LTC4 and LTD4, are involved in the pathogenesis of asthma and other allergic diseases.
- Thromboxanes (TXs): Thromboxanes are produced by platelets and have important roles in blood clotting and vasoconstriction. Thromboxane A2 (TXA2) promotes platelet aggregation and constriction of blood vessels, contributing to the formation of blood clots. In inflammation, thromboxanes can also modulate immune cell activation and recruitment.
The synthesis and activity of eicosanoids are tightly regulated by enzymes and receptors. The enzymes involved in eicosanoid synthesis are cyclooxygenases (COX) for prostaglandins and thromboxanes, and lipoxygenases (LOX) for leukotrienes. The COX enzymes exist in two isoforms, COX-1 and COX-2, which have distinct roles in inflammation and homeostasis. The receptors for eicosanoids are G protein-coupled receptors (GPCRs) located on the surface of target cells. Each eicosanoid utilizes specific receptors to exert its biological effects.
Regulators of eicosanoid synthesis and activity include anti-inflammatory drugs, such as nonsteroidal anti-inflammatory drugs (NSAIDs) that inhibit COX enzymes, and corticosteroids that suppress the synthesis of eicosanoids. Additionally, dietary factors, such as omega-3 fatty acids found in fish oils, can influence eicosanoid production and modulate inflammation.
Understanding the roles of eicosanoids and their regulators is crucial for comprehending the complex mechanisms underlying inflammation and developing therapeutic interventions targeting eicosanoid pathways in various inflammatory diseases.
Fig.1 The role of eicosanoids in the mediation of inflammation and resolution through class-switching and thus in the maintenance of homeostasis. (Mohammed A, et al., 2022)
Common Inflammation and Eicosanoids and Regulators
Eicosanoids and their regulators have a strong association with the inflammatory response, as they play critical roles in initiating, amplifying, and resolving inflammation. The synthesis, release, and signaling of eicosanoids are tightly regulated by enzymes, receptors, and other regulatory proteins. Here is a detailed introduction to the association between eicosanoids, their regulators, and inflammation:
Eicosanoid synthesis and release
- Arachidonic acid release: In response to stimuli like tissue injury or immune activation, phospholipases are activated, leading to the release of arachidonic acid from cell membrane phospholipids. Arachidonic acid serves as a precursor for the synthesis of eicosanoids.
- Enzymatic conversion: Arachidonic acid is converted into various eicosanoids by specific enzymes. Cyclooxygenases (COX) convert arachidonic acid into prostaglandins and thromboxanes, while lipoxygenases (LOX) convert them into leukotrienes and lipoxins. These enzymatic conversions occur in different cell types, including immune cells, endothelial cells, and platelets.
- Release and activation: Upon synthesis, eicosanoids are released into the extracellular environment. They act locally on nearby cells or, in some cases, exert systemic effects by entering the bloodstream.
Pro-inflammatory effects of eicosanoids
- Vasodilation and vascular permeability: Prostaglandins, particularly prostaglandin E2 (PGE2), induce vasodilation and increase vascular permeability. This allows immune cells and other inflammatory mediators to migrate from the bloodstream to the site of inflammation.
- Immune cell recruitment: Eicosanoids, such as leukotriene B4 (LTB4), attract and activate immune cells, including neutrophils and monocytes, to the site of inflammation. These cells are essential for initiating the inflammatory response and clearing pathogens.
- Cytokine modulation: Prostaglandins and other eicosanoids can regulate the production of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha) and interleukins, which further amplify the inflammatory response.
Resolution of inflammation
- Anti-inflammatory eicosanoids: Some eicosanoids, such as lipoxins and certain prostaglandins (e.g., prostaglandin E1 and prostaglandin D2), have anti-inflammatory properties. They promote the resolution of inflammation by inhibiting the production of pro-inflammatory cytokines, reducing immune cell recruitment, and promoting tissue repair.
- Regulators of eicosanoid synthesis: Regulatory proteins, including fatty acid-binding proteins (FABPs) and phospholipases, modulate the availability of arachidonic acid and the activity of enzymes involved in eicosanoid synthesis. These regulators can influence the balance between pro-inflammatory and anti-inflammatory eicosanoids.
Feedback regulation
- Negative feedback loops: Some eicosanoids and their downstream signaling pathways can activate negative feedback mechanisms to prevent excessive inflammation. For example, prostaglandin E2 can inhibit the production of inflammatory mediators and promote the production of anti-inflammatory cytokines.
- Resolution mediators: As inflammation progresses, specialized pro-resolving lipid mediators (SPMs), such as resolvins, protectins, and maresins, are produced from eicosanoids. These SPMs actively promote the resolution of inflammation, facilitate tissue repair, and prevent chronic inflammation.
The association between eicosanoids, their regulators, and inflammation is highly complex and dynamic. Imbalances or dysregulation in the production, release, or signaling of eicosanoids can lead to chronic inflammation and contribute to the development of inflammatory diseases. Understanding the interplay between eicosanoids and their regulators is vital for developing targeted therapies aimed at modulating the inflammatory response and restoring homeostasis in inflammatory disorders.
Fig.2 Eicosanoid metabolism and its relevance in inflammation. (Brücher B L D M, et al., 2019)
References:
- Esser-von Bieren, Julia. "Immune-regulation and -functions of eicosanoid lipid mediators" Biological Chemistry, vol. 398, no. 11, 2017, pp. 1177-1191. https://doi.org/10.1515/hsz-2017-0146
- Philip C. Calder; Eicosanoids. Essays Biochem 23 September 2020; 64 (3): 423–441. doi: https://doi.org/10.1042/EBC20190083
- Mohammed A, Kalle AM, Reddanna P. Managing SARS-CoV2 Infections Through Resolution of Inflammation by Eicosanoids: A Review. J Inflamm Res. 2022;15:4349-4358. Published 2022 Jul 29. doi:10.2147/JIR.S355568
- Brücher B L D M, Jamall I S. Eicosanoids in carcinogenesis[J]. 4open, 2019, 2: 9.
