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The Human Immune System Seen from a Biomedical Engineering Viewpoint
Published in Robert B. Northrop, Endogenous and Exogenous Regulation and Control of Physiological Systems, 2020
Platelet-activating factor (PAF) is synthesized by platelets, mast cells, macrophages, eosinophils, certain renal cells, and vascular endothelial cells. The PAF molecule is shown in Figure 10.5. PAF is a pharmacologically active autacoid with many diverse functions.61 It causes vasodilation and it is over 1000 times more effective than histamine or bradykinin in promoting edema. PAF promotes platelet aggregation in vitro and in vivo and is a chemotactic factor for eosinophils, neutrophils, and monocytes, causing these leukocytes to aggregate at the source of its release. PAF also causes the contraction of smooth muscles in the gastrointestinal tract, the small airways, and the uterus. PAF certainly contributes to the edema which occurs when the immune system fights a bacterial infection introduced through the skin.
Immune Modulation by Dermal Exposure to Jet Fuel
Published in Mark L. Witten, Errol Zeiger, Glenn D. Ritchie, Jet Fuel Toxicology, 2010
Gerardo Ramos, Stephen E. Ullrich
An early step in jet-fuel-induced immune suppression is the production of PGE2 by JP-8-treated keratinocytes (Ramos et al., 2004). A critical step in PGE2 secretion, and perhaps one of the earliest steps in the cascade of events leading to immune suppression is the secretion of the lipid mediator of inflammation, PAF. As its name implies, PAF activates a wide variety of cells, including platelets, monocytes, mast cells, and polymorphonuclear leukocytes. In addition to activating platelets, it also activates monocytes, mast cells, and polymorphonuclear leukocytes. PAF plays a role in cell communication. Cells that are responsive to PAF express a seven transmembrane spanning G-coupled protein receptor. Binding of PAF to its receptor activates a variety of intracellular events, such as increased calcium flux, activation of mitogen-activated protein kinase pathways, activation of phospholipase (PLA2), and transcriptional activation of a variety of genes, including COX-2 (Ishii and Shimizu, 2000) and IL-10 (Walterscheid, Ullrich, and Nghiem, 2002). PAF is secreted in response to oxidative stress, and is secreted by epidermal cells almost immediately following skin trauma (Alappatt et al., 2000). Because PAF up-regulates the production of PGE2 (Pei et al., 1998), we tested the hypothesis that JP-8-induced PAF activates cytokine production and initiates immune suppression. We pretreated jet-fuel-treated mice with a series of PAF receptor antagonists. Injecting the PAF receptor antagonists totally reversed jet-fuel-induced immune suppression. We noted reversal of immune suppression regardless of whether Jet A or JP-8 was used. At the cellular level, we observed that pretreating JP-8 or Jet-A-treated keratinocytes with a PAF receptor antagonist blocked PGE2 secretion. We also found that treating jet-fuel-exposed mice with antioxidants, such as Vitamin C, Vitamin E, and beta-hydroxyl toluene (BHT), blocked immune suppression (Ramos et al., 2004). Because jet fuel treatment induces oxidative stress (Rogers et al., 2001), which has been associated with increased PAF production (Alappatt et al., 2000), these findings support the hypothesis that PAF production is an essential and early step in the cascade of effects leading to JP-8- and Jet-A-induced immune suppression. We propose that jet-fuel-induced PAF induces keratinocytes to secrete PGE2, which then activates a cascade of events, including IL-10 secretion as described previously (Shreedhar et al., 1998), that ultimately suppresses cell mediated immune reactions, such as DTH, CHS, and T cell proliferation.
Updating futsal physiology, immune system, and performance
Published in Research in Sports Medicine, 2022
Leandro Borges, Alexandre Dermargos, Renata Gorjão, Maria F. Cury-Boaventura, Sandro M. Hirabara, Cesar C. Abad, Tania C. Pithon-Curi, Rui Curi, Marcelo P. Barros, Elaine Hatanaka
Injury due to local trauma or repetitive overload impairs neuromuscular and proprioceptive activities of the limbs. In general, there is a decrease in performance due to pain, swelling, heat, redness, ischaemia, muscle tension, and impaired muscle reflex contraction (Chazaud, 2016), and chemical mediators released by leukocytes trigger these symptoms. Natural killer cells, endothelial cells, mast cells, and platelets cause vasodilatation, inducing an increase in vessel permeability and the chemotaxis of leukocytes, mainly monocytes, and neutrophils to the inflammatory site (Hyldahl et al., 2017). During inflammation, there is also a release of vasoactive amines (histamine), mediators derived from phospholipids (prostaglandins, thromboxanes, leukotrienes, and platelet-activating factor), bradykinin, nitric oxide, tumour-necrosis-factor alpha, interleukin (IL)-1b, IL-6, and IL-8 (Peake et al., 2017). These mediators orchestrate the whole inflammatory response to prompt tissue repair and recovery.
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
In this disorder, individuals with existing metal sensitivity namely Ni allergy prior to the implantation of metal-containing endovascular devices, or subjects that become subsequently sensitized after device implantation, are likely to experience chronic allergic irritation to the coronary intima (Koniari, Kounis, and Hahalis 2016; Kounis 2016). As a result, stented areas tend to become populated by increasing numbers of mast cells and other inflammatory cells. Subsequent release of metal ions from the stent lead to activation of localized mast cells and the corresponding release of mediators including histamine, chemokines, arachidonic acid metabolites, platelet-activating factor, and neural proteases – many of which exert potent effects on the cardiovascular system that might trigger activation of the coronary component involved in Kounis syndrome (Kounis 2013).
PEGylated liposomes: immunological responses
Published in Science and Technology of Advanced Materials, 2019
Marwa Mohamed, Amr S. Abu Lila, Taro Shimizu, Eman Alaaeldin, Amal Hussein, Hatem A. Sarhan, Janos Szebeni, Tatsuhiro Ishida
As described above, intravenous injections of lipid-containing therapeutics could trigger adverse immunological reactions through complement activation via both the classical and the alternative pathways, resulting in CARPA [21,76,87]. The exact mechanism of liposome-induced CARPA is still being elucidated as it involves many cellular (including secretory cells, blood cells and effector cells) and molecular processing (including anaphylotoxins and allergomedins). The working hypothesis is that, upon complement activation, anaphylatoxins such as C5a and C3a are released, and they activate macrophages, basophils and mast cells through their specific receptors. These cells then secrete a variety of vasoactive inflammatory mediators, referred to as allergomedins, involving tryptase, histamine, platelet-activating factor (PAF) and leukotrienes (LTB2, LTD4, LTC4, PGD2, TXA2 and LTE4) [21,91] as shown in Figure 3. When the complement system is activated, some of these allergomedins (histamine, PAF, TAX2 and tryptase) are released from the cells. The released mediators bind to their receptors on autonomic effector cells such as endothelial cell and smooth muscle cells, causing their activation, resulting in CARPA [92].