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Epithelial Cells
Published in Bruce S. Bochner, Adhesion Molecules in Allergic Disease, 2020
Mammalian respiratory epithelia are characterized by the 5-, 12-, and 15-lipoxygenase pathways (198), the last of which predominates in the human host (201). The 15-lipoxygenase enzyme converts arachidonic acid to the metabolically important 15-hydroxyeicosatetraenoic acid (15-HETE) and a broad range of hydroperoxy-, epoxyhydroxy-, keto-, and dihydroxy-acids (199,201). Murray et al. (202) were the first to report significant levels of 15-HETE in the BAL fluids of chronic stable asthmatics subjected to antigen provocation. It was not clear, however, that airway epithelial cells were the source of this metabolite because eosinophils also contain high levels of 15-lipoxygenase (203). Activity of 15-lipoxygenase has since been shown to be increased in asthmatic bronchial epithelium by both metabolic assay (204) and direct immunohistochemical staining (205).
Inflammation resolution and specialized pro-resolving lipid mediators in chronic rhinosinusitis
Published in Expert Review of Clinical Immunology, 2023
Peyton Z. Robinson, Daniel N. Frank, Vijay R. Ramakrishnan
Mechanisms by which arachidonic acid-derived lipoxins promote resolution of inflammation include: reduction of neutrophil chemotaxis in response to leukotriene B4 and prostaglandins, increasing monocyte infiltration and vascular permeability, inhibiting production of reactive oxygen species, and stimulating clearance of apoptotic neutrophils by macrophages (Table 1) [50,54]. Lipoxin A4 (LXA4) and Lipoxin B4 (LXB4) are synthesized through two established pathways: 1) by 15-Lipoxygenase (15-LOX) and 5-Lipoxygenase (5-LOX), with 15-hydroxyeicosatetraenoic acid (15-HETE) as the intermediate or 2) using 5-LOX and 12-Lipoxygenase (12-LOX) with 5-hydroxyeicosatetraenoic acid (5-HETE) as the intermediate [52]. 15-HETE is also a stable intermediate that can be reliably assayed, and has pro-resolving capabilities similar to lipoxins [53].
Targetting ferroptosis for blood cell-related diseases
Published in Journal of Drug Targeting, 2022
Zhe Chen, Jinyong Jiang, Nian Fu, Linxi Chen
The existing protein–protein interaction network analysis shows that B-cell receptor signalling and immunodeficiency intestinal IgA production may be closely related to ferroptosis [35]. Gpx4 inhibitor RSL3 can induce ferroptosis in B lymphocytes from patients with mitochondrial disease-associated epilepsy [63]. However, EPI-743, an α-tocotrienol quinone, alleviates seizure frequency in children with the mitochondrial disorder-related epilepsy. Specifically, EPI-743 can also inhibit ferroptosis and induce a cytoprotection by a dose-dependent decrease in general lipid oxidation and the specific 15-lipoxygenase (15-LO) product 15-hydroxyeicosatetraenoic acid (15-HETE) in the mitochondrial disease-related epilepsy. In addition, a recent study demonstrates that ferroptosis is involved in the development and homeostasis of innate-like B1-cells which regulate an efficient antibody responses [64]. Mechanically, ferroptosis induced by Gpx4 deficiency can mediate the B1 and marginal zone (MZ) B cells death to impair B cell development. By contrast, inhibiting ferroptosis with Gpx4 is essential for B-cells development and antibody responses to Streptococcus pneumoniae. However, ferroptosis is not necessary but dispensable for follicular B2-cells development and antibody responses. The development and differentiation of B2-cells might be related to cellular other antioxidant pathway like Nrf2 signal pathway [65]. Notably, it hints that ferroptosis may mediate the difference of B2-cells into functional B cells.
Silicone hydrogel contact lenses retain and document ocular surface lipid mediator profiles
Published in Clinical and Experimental Optometry, 2023
Karsten Gronert, Arnav Modi, Kaleb Asfaha, Sharon Chen, Elizabeth Dow, Scott Joslin, Mike Chemaly, Zohra Fadli, Leilani Sonoda, Bailin Liang
Current knowledge of lipid mediators in the eye and their actions in other organs/tissues3,4,6,7,10,34 enables some preliminary interpretation of the silicone hydrogel lens lipidomic profiles. 15-hydroxyeicosatetraenoic acid and 17-hydroxydocosahexaenoic acid are pathway markers for the production of lipoxin A and DHA-derived resolvins, respectively. These specialized proresolving mediator intermediates are generated by 15-lipoxygenase an enzyme that is highly expressed in corneal epithelial cells and immune-regulatory leukocytes. 12-hydroxyeicosatetraenoic acid and 14-hydroxydocosahexaenoic acid are markers for 12-lipoxygenase activity. Expression of 12-lipoxygenase in humans is cell specific and in general a marker of inflammation. The cellular source of 12-lipoxygenase in the ocular surface in humans is currently unknown. 5- hydroxyeicosatetraenoic acid and leukotriene B4 are products of the 5-lipoxygenase pathway, which is expressed by several cell types in the ocular surface. However, leukotriene B4 formation in the ocular surface appears to be limited to recruited neutrophils that respond to infection.25 Hence, leukotriene B4 that was generated in selected subjects, likely reflects an early pre-clinical neutrophil microbial response. Antibody-based analyses has documented immuno-reactive leukotriene B4 in human tears with contact lens wear suggesting a potential link to a contact lens-induced inflammation.13 Prostaglandin E2 formation is initiated by cyclooxygenase enzymes that can be expressed by many cells in the ocular surface and prostaglandin E2 is markedly increased in response to chronic corneal injury.33 Based on evidence from corneal injury animal models and the clinical efficacy of topical nonsteroidal anti-inflammatory drugs, prostaglandin E2 has significant roles in amplifying pain and inflammation in the ocular surface. Hence, increased level of prostaglandin E2 may be an early response to adverse effects of contact lens wear.