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Abstract
Arachidonic acid (AA) metabolism is critical in the initiation and resolution of inflammation. Prostaglandin E2 (PGE2) and leukotriene B4/D4/E4 (LTB4/LD4/LTE4), derived from AA, are involved in the initiation of inflammation and regulation of immune response, hematopoiesis, and M1 (pro-inflammatory) macrophage facilitation. Paradoxically, PGE2 suppresses interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) production and triggers the production of lipoxin A4 (LXA4) from AA to initiate inflammation resolution process and augment regeneration of tissues. LXA4 suppresses PGE2 and LTs’ synthesis and action and facilitates M2 macrophage generation to resolve inflammation. AA inactivates enveloped viruses including SARS-CoV-2. Macrophages, NK cells, T cells, and other immunocytes release AA and other bioactive lipids to produce their anti-microbial actions. AA, PGE2, and LXA4 have cytoprotective actions, regulate nitric oxide generation, and are critical to maintain cell shape and control cell motility and phagocytosis, and inflammation, immunity, and anti-microbial actions. Hence, it is proposed that AA plays a crucial role in the pathobiology of ischemia/reperfusion injury, sepsis, COVID-19, and other critical illnesses, implying that its (AA) administration may be of significant benefit in the prevention and amelioration of these diseases.
Highlights
It is suggested that Arachidonic acid (AA) and its metabolites may have a therapeutic role in the prevention and management of ischemia/reperfusion injury, sepsis, COVID-19, ARDS, and other critical illnesses, with emphasis on COVID-19
COVID-19 is like other respiratory viral diseases such as influenza and infects and induces apoptosis of T lymphocytes to induce severe lymphopenia and impair lymphopoiesis partly due to a striking reduction in Bcl-6+ germinal center B cells that correlate with an early specific block in Bcl-6+ TFH cell differentiation associated with an increase in Tbet+ TH1 cells and aberrant extrafollicular tumor necrosis factor-α (TNF-α) accumulation in the spleen and lymph nodes [4]. These results suggest that the high TNF-α levels seen in severe COVID-19 cause a so-called ‘cytokine storm’, which is rather controversial [5], and suppress immune response, leading to a lack of type I IFNs, reduced HLA-DR in the myeloid cells, and transient expression of IFN-stimulated genes [6,7]
In all probability, lipoxin A4 (LXA4) is more potent in suppressing the production of IL-6 and TNF-α compared to resolvins and protectins, especially in streptozotocin-induced type1 and type 2 diabetic models [13,14,15]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Some of the serious illnesses in which inflammation plays a critical role include ischemia/reperfusion injury, sepsis, ARDS (acute respiratory distress syndrome), post-surgical sepsis/shock, and cytokine storm seen in patients with COVID-19. In all these conditions, acute inflammation goes unabated due to excess production of pro-inflammatory cytokines, prostaglandins, leukotrienes, bradykinin, and reactive oxygen species (ROS). Biomolecules 2021, 11, 1873 and ARDS and the potential role of bioactive lipids and their pro- and anti-inflammatory metabolites Based on this evidence, it is suggested that AA and its metabolites may have a therapeutic role in the prevention and management of ischemia/reperfusion injury, sepsis, COVID-19, ARDS, and other critical illnesses, with emphasis on COVID-19
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