Modulation of the PMN Leukocyte Component of Hypersensitivity Reactions by Lipoxygenase Products of Arachidonic Acid

Goetzl, Edward J.; Derian, Claudia K.; Owens, Caroline; Valone, Frank H.

doi:10.1016/b978-0-08-026384-7.50040-9

Cited by 8 publications

(6 citation statements)

References 24 publications

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“…However, when arachidonic-acid-containing plasmalogens are under oxidative stress, they become precursors of arachidonic-derived lipid mediators such as leukotrienes and hydroxyeicosatetraenoic acids [29],[31],[35],[36]. These reactive lipids are important mediators of inflammatory response [37]. Thus, this remodeling process occurring in the membranes may make the adipocytes more vulnerable and prone to inflammatory responses (Figure 7), in agreement with the elevation of inflammatory pathways in the obese twins of weight-discordant twin pairs [12].…”

Section: Discussionmentioning

confidence: 99%

Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans

et al. 2011

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“…and trigger the ROS stress [198]. The product LTs are complementary pro-inflammatory factors to the PGE2.…”

Section: Arachidonic Acid Metabolism Pathway and Inflammationmentioning

confidence: 99%

Inflammation, Fibrosis and Cancer: Mechanisms, Therapeutic Options and Challenges

Sodji

Oyelere

2022

Cancers

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Uncontrolled inflammation is a salient factor in multiple chronic inflammatory diseases and cancers. In this review, we provided an in-depth analysis of the relationships and distinctions between uncontrolled inflammation, fibrosis and cancers, while emphasizing the challenges and opportunities of developing novel therapies for the treatment and/or management of these diseases. We described how drug delivery systems, combination therapy and the integration of tissue-targeted and/or pathways selective strategies could overcome the challenges of current agents for managing and/or treating chronic inflammatory diseases and cancers. We also recognized the value of the re-evaluation of the disease-specific roles of multiple pathways implicated in the pathophysiology of chronic inflammatory diseases and cancers—as well as the application of data from single-cell RNA sequencing in the success of future drug discovery endeavors.

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“…Arachidonic acid (C20:4) released by phospholipases from cell membrane is metabolized by lipoxygenases (LOX); especially, 5-LOX generates 5-HETE and leukotriene B 4 from arachidonic acid (C20:4) (Harizi et al, 2008). These two metabolites induce chemotactic response and chemokinesis of leukocytes and show increased levels in inflammatory lesions for immune function, therefore, 5-HETE and leukotriene B 4 may play a key role on leukocyte function (Goetzl et al, 1982). In the present study, leukotriene B 4 and 5-HETE levels were significantly lower in the LC group than the control group and the leukocyte number in the LC group had a trend toward decrease compared to the control group.…”

Section: Discussionmentioning

confidence: 99%

Liver Cirrhosis Patients Who Had Normal Liver Function Before Liver Cirrhosis Development Have the Altered Metabolic Profiles Before the Disease Occurrence Compared to Healthy Controls

Yoo

Kim

et al. 2019

Front. Physiol.

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Liver cirrhosis (LC) is the final usual outcome of liver damage induced by various chronic liver diseases. Because of asymptomatic nature of LC, it is usually diagnosed at late and advanced stages, and patients are easy to miss the best timing for treatment. Thus, the early detection of LC is needed. In the prospective Korean Cancer Prevention Study-II (K-II), we aimed to identify valuable biomarkers for LC using metabolomics to distinguish subjects with incident LC (LC group) from subjects free from LC (control group) during a mean 7-year follow-up period. Metabolic alterations were investigated using baseline serum specimens acquired from 94 subjects with incident LC and 180 age- and sex-matched LC-free subjects via ultra-performance liquid chromatography (UPLC)-linear-trap quardrupole (LTQ)-Orbitrap mass spectrometry (MS). As a result of the metabolic analysis, 46 metabolites were identified. Among them, 11 and 18 metabolite level showed a significant increase and decrease, respectively, in the LC group compared to the control group. Nine metabolic pathways, including glyoxylate and dicarboxylate metabolism, amino acid metabolism, fatty acid metabolism, linoleic acid metabolism, α-linolenic acid metabolism, and arachidonic acid metabolism, were significantly different between the two groups. Logistic regression demonstrated that the LC emergence was independently affected by serum levels of myristic acid, palmitic acid, linoleic acid, eicosapentaenoic acid (EPA), lysophosphatidic acid (LPA) (18:1), glycolic acid, lysophosphatidylcholine (lysoPC) (22:6), and succinylacetone (R2 = 0.837, P < 0.001). This prospective study revealed that dysregulation of various metabolism had the clinical relevance on the LC development. Moreover, myristic acid, palmitic acid, linoleic acid, EPA, LPA (18:1), glycolic acid, lysoPC (22:6), and succinylacetone were emerged as independent variables influencing the incidence of LC. The results support that the early biomarkers found in this study may useful for predicting and remedying the risk of LC.

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Modulation of the PMN Leukocyte Component of Hypersensitivity Reactions by Lipoxygenase Products of Arachidonic Acid

Cited by 8 publications

References 24 publications

Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans

Association of Lipidome Remodeling in the Adipocyte Membrane with Acquired Obesity in Humans

Inflammation, Fibrosis and Cancer: Mechanisms, Therapeutic Options and Challenges

Liver Cirrhosis Patients Who Had Normal Liver Function Before Liver Cirrhosis Development Have the Altered Metabolic Profiles Before the Disease Occurrence Compared to Healthy Controls

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