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The Role of Platelet-Activating Factor in the Pathogenesis of Necrotizing Enterocolitis
Published in David J. Hackam, Necrotizing Enterocolitis, 2021
Platelet-activating factor (PAF) is an endogenous phospholipid mediator with multiple potent effects (1). It was known in the late 1970s that a compound was present in the circulation and tracheal fluid that resulted in platelet aggregation and degranulation, and by 1979, Benveniste and others identified this molecule as an acyl glycolipid that they called PAF (2). This glycolipid was shown to have a very short half-life in vivo and was present in most cells, fluids, and tissues (3). PAF is synthesized following the hydrolysis of phosphatidylcholine by phospholipase A2 into lyso-PAF with the following acetyl-transferase conversion into PAF. Lyso-PAF has minimal biologic activity, though PAF has potent effects following ligand binding to the PAF receptor that is present on most cells and tissues. PAF is converted back to the inactive lyso-PAF by the enzyme PAF-AH, and as discussed later in this chapter, this important enzyme is relatively deficient in the newborn circulation (4). It has been suggested that endogenous PAF functions in part to protect the intestine from invasive pathogen exposure by activating an intense self-limited inflammatory response. If the organism or local environment lacks appropriate PAF-AH activity to down-regulate PAF activation, severe intestinal necrosis may result.
Herbal Supplements and Health
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
Himangini Bansal, Sakshi Bajaj
The flavoglycosides present in ginkgo are its most active component and have shown surprising pharmacological capacities. These chemical compounds have free radical properties and act as an antioxidant agent. These flavonoids consist of kaempferol, isorhamnetine, and quercitin. The terpene substance of ginkgo, which incorporates the ginkgolides and the bilobalides, helps to reduce inflammation by inhibiting platelet activating factor (PAF) in the blood. This activity facilitates to reinforce circulation. PAF assumes a role in various disease, for example, heart attacks, strokes, atherosclerosis, and asthma (Nash and Shah, 2015).
The Role of Platelet-Activating Factor in Endotoxin-Related Disease
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Taco W. Kuijpers, Tom van der Poll
Platelet-activating factor (PAF) is a phospholipid implicated in various pathophysiological conditions. Its mediator role was originally identified in anaphylaxis and allergic diseases such as asthma. Recent studies suggest a broader role for PAF in inflammatory reactions, such as sepsis, acute respiratory distress syndrome (ARDS), disseminated intravascular coagulation (DIC), necrotizing pancreatitis, hemolytic uremic syndrome, and IL-2 immunotherapy (1–11). The potent bioactivity of PAF towards cells depends on its structural features (Fig. 1A), with an ether linkage at the sn-1 position and an acetate at the sn-2 position (1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphocholine) (1,2,12). The precursor lipid for PAF is l-O-alkyl-2-acyl-glyceryl-3-phosphocholine (GPC), an alkoxyether phospholipid present in the plasma membrane of most cell types. The key enzymes involved in the biosynthesis of GPC are localized in peroxisomes. Once formed, GPC is transferred to the plasma membrane. During inflammation, the rapid formation of PAF from cellular membranes takes place by the enzymatic activity of cytoplasmic phospholipase A2 (cPLA2) and acetyltransferase, both activated upon cellular stimulation (1,2,13). PAF can be produced in response to injury by various cells, including endothelial cells, macrophages, granulocytes, and platelets (1,2).
Evaluation of maternal plasma platelet activating factor acetylhydrolase activity and mRNA expression in pre-eclampsia: a case control study
Published in Journal of Obstetrics and Gynaecology, 2021
Preeti Gupta, Rachna Agarwal, Sruthi Bhaskaran, Seema Garg, Mohit Mehndiratta, Gita Radhakrishnan, Alpana Singh, Richa Agarwal, Divya Narang
Preeclampsia is a complication of pregnancy closely related to placental dysfunction. Platelet-activating factor (PAF) is a biologically potent Ether phospholipid, generated by many types of cells including neutrophils, monocytes/macrophages, platelets, and endothelial cells (Prescott et al. 2000). PAF-like oxidised phospholipids are oxidatively modified phospholipids that could be produced by oxidative stress. Both PAF and PAF-like oxidised phospholipids are potent proinflammatory mediators, production and accumulation which are associated with various inflammatory diseases such as asthma, sepsis, cardiac infarction, cerebral ischaemia, and hypertension (Karasawa 2006). In this observational case-control study we made an effort to understand the pathogenesis of preeclampsia using PAF-AH, as the aetiology and pathogenesis remain elusive.
The clinical evidence of second-generation H1-antihistamines in the treatment of allergic rhinitis and urticaria in children over 2 years with a special focus on rupatadine
Published in Expert Opinion on Pharmacotherapy, 2021
Antonio Nieto, María Nieto, Ángel Mazón
Although histamine is the main mediator in the pathophysiology of allergic rhinitis and chronic urticaria, it is clearly not the only mediator involved in these processes. In recent years, the role of platelet activating factor (PAF) as a key mediator involved in the allergic hypersensitivity reaction has gained recognition. PAF is an endogenous phospholipid synthesized in inflammatory cells such as mast cells, eosinophils, basophils, neutrophils, macrophages, and platelets, which is released during allergic or inflammatory reactions. In allergic rhinitis, these reactions are associated with increased vascular permeability, eosinophil chemoattraction, and airway hyperresponsiveness. Increased plasma levels of PAF have been reported in patients with urticaria compared with healthy controls [12–17]. Additionally, recent findings in CSU patients, particularly those with sgAH refractoriness, showed significant increases in serum PAF levels and decreases in PAF-AH. Therapies modulating PAF and PAF-acetylhydrolase (PAF-AH), which is responsible for PAF degradation. PAF-AH levels could be effective in patients with CSU refractory to antihistamines [18].
Occupational lung diseases
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2020
A detailed American Thoracic Society and European Respiratory Society official statement, published in 2019,1 estimated the occupational burden of several nonmalignant chronic lung diseases. The highest occupational population attributable fraction (PAF) was for idiopathic pulmonary fibrosis, estimated as 26%. However, the authors note the potential for misclassification, firstly, in diagnosis as some patients may have had hypersensitivity pneumonitis or pneumoconiosis such as silicosis or asbestosis, causing overestimation of PAF; and secondly, the potential for exposure misclassification such as possible underestimation of exposure to asbestos based on patient history, causing potential misattribution to other work agents. The PAF was 13–16% for asthma, chronic obstructive pulmonary disease and chronic bronchitis, similar to previous estimates. For diseases where there were insufficient studies to determine PAF, the estimated occupational burden was 30% for granulomatous diseases including sarcoidosis, 29% for pulmonary alveolar proteinosis and 19% for hypersensitivity pneumonitis, with lower estimates for tuberculosis and community acquired pneumonia. These estimates emphasize the need to consider occupational diseases among all adult patients with respiratory disease: the occupational cause will often not be suspected unless an occupational history is taken.