China
Africa
Explore chapters and articles related to this topic
In vitro Testing for Adverse Drug Reactions
Published in Kirsti Kauppinen, Kristiina Alanko, Matti Hannuksela, Howard Maibach, Skin Reactions to Drugs, 2020
Human basophils play an important role in diverse inflammatory processes. They generate de novo leukotriene C4, and the generation can be enhanced in the presence of interleukin-3 both upon IgE-dependent and IgE-independent basophil degranulation.29 A commercial test (by Bühlmann laboratories AG, Allschwil, Switzerland) takes advantage of this release of sulfidoleukotrienes in vitro. Czech et al.30 showed that leukocytes from patients with a pseudo-allergic reaction to acetylsalicylic acid released significantly larger amounts of sulfidoleukotrienes upon stimulation with C5a man leukocytes from controls. Bircher et al.31 showed preliminary results suggesting that patients with anaphylactic reaction to beta-lactam antibiotics could be diagnosed with in vitro release of sulfidoleukotrienes, while patients with milder skin eruptions remained negative in the test.
Molecular Mechanisms Controlling Immunoglobulin E Responses
Published in Thomas F. Kresina, Immune Modulating Agents, 2020
Rachel L. Miller, Paul B. Rothman
Whereas IL-4 is critical to IgE production, another type 2 cytokine, IL-5, acts as a differentiation and growth factor for eosinophils during allergic disease. Interleukin-5, IL-3, and GM-CSF all induce eosinophil production, as demonstrated in both in vitro and in vivo experiments [44], but only IL-5 is specific for the eosinophil lineage. The IL-5 stimulates eosinophilopoiesis in the bone marrow [45] and promotes the terminal differentiation of myeloid precursors into eosinophils [46]. Eosinophils play an essential role during allergic diseases and parasitic infections by releasing eosinophil-derived proteins such as major basic protein (MBP) and the eosinophilic cationic protein (ECP). In helminthic and parasitic infections, the eosinophilie-derived granules are believed to be toxic to the infesting cells. In asthma, epithelial shedding is believed to result from the release of eosinophil major basic protein [47], and mucus hypersecretion and airway hypereactivity are believed to be consequences of the release of the eosinophil and mast cell-derived leukotriene C4, which is cleaved to the active products leukotriene D4 and E4 [48]. In addition, IL-5 promotes the migration of eosinophils from the blood to the tissues in response to antigen challenge [49,50] and increases eosinophil, but not neutrophil, adhesion to vascular endothelium [51]. Although IL-5 does not contribute to IgE production, the Th2 immune response that promotes IL4, IL-13, and IL-5 secretion, all contribute to the inflammation-related symptoms in complementary ways.
Platelet-Activating Factor Receptors in the Airways
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
PAF-acether can cause microvascular leakage and edema.126 PAF-acether is also an effective chemoattractant and activator of eosinophils in vitro.23,171–175 So far, PAF-acether is the most potent chemotactic factor for eosinophils. In vivo, there is recruitment of eosinophils into the lung following intratracheal administration of PAF-acether in primates or intravenous administration of PAF-acether in guinea pigs. Recent studies more closely associate eosinophils with airway hyperresponsiveness by the elaboration of cytotoxic and neurotoxic mediators which may damage bronchial mucosa, such as is found in airways of subjects with bronchial asthma.169,176 The cytotoxic and neurotoxic mediators released from eosinophils include eosinophil peroxidase, major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin. Leukotriene C4 and superoxide radicals are also released from eosinophils in response to PAF-acether,172–175,177–179 and these mediators can cause tissue inflammation in allergy and asthma. This has been discussed in greater details in the previous chapter on eosinophils by Makino and colleagues (see Chapter 7).
Possible therapeutic effects of Nigella sativa and its thymoquinone on COVID-19
Published in Pharmaceutical Biology, 2021
Mohammad Reza Khazdair, Shoukouh Ghafari, Mahmood Sadeghi
Administration of TQ (3 mg/kg, i.p.) decreased the production of leukotriene B4 (LTB4) and leukotriene C4 (LTC4) in the BALF of mice. Furthermore, the levels of IL-4, IL-5, and IL-13 were also significantly decreased while IL-10 was increased when TQ administered before OVA challenge (El Gazzar, El Mezayen, Nicolls et al. 2006). Similarly, TQ (3 mg/kg, i.p.) significantly decreased elevated serum levels of IgE and IgG1 and also inhibited allergen induced lung inflammation and production of mucus by goblet cells. TQ also significantly inhibited IL-4, IL-5, and IL-13 but increased IFN-γ production in the BALF. In addition, a small effect of TQ was observed on the production of IL-4 in OVA-stimulated cultured lung cells. These results indicated the effect of TQ on reduction of airway inflammation (inhibition of eosinophil infiltration into the airways) and Th2 cytokines productions (El Gazzar, El Mezayen, Marecki et al. 2006). Intraperitoneal administration of TQ (5 or 10 mg/kg) 30 min before LPS injection (1 mg/kg i.p.) decreased the levels of IL-6 and TNF-α in treated rats (Bargi et al. 2017). Orally administration of TQ (10, 20, and 40 mg/kg/day, p.o.) for 14 days after Alzheimer’s disease (AD) induction in rats, decreased amyloid-β (Aβ) formation and accumulation, and also reduced the levels of TNF-α and IL-1β. Furthermore, it significantly down regulated the expression of NF-κB and interferon regulatory factor 3 (IRF-3) mRNAs (Abulfadl et al. 2018).
Immunological mechanisms underlying chronic rhinosinusitis with nasal polyps
Published in Expert Review of Clinical Immunology, 2018
Enrico Heffler, Luca Malvezzi, Monica Boita, Luisa Brussino, Armando De Virgilio, Matteo Ferrando, Francesca Puggioni, Francesca Racca, Niccolò Stomeo, Giuseppe Spriano, Giorgio Walter Canonica
Another immunological mechanism that is enhanced at least in a proportion of patients with CRSwNP (namely those with nonsteroidal anti-inflammatory drugs – NSAIDs – hypersensitivity [57]) is the baseline overproduction of cysteinyl leukotrienes via the 5-lipoxygenase pathway, exacerbated by ingestion of aspirin or other NSAIDs with anti-cyclo-oxygenase-1 (COX-1) activity. Typically, this immunological mechanism is associated with CRSwNP and eosinophilic phenotype of asthma, being this syndrome the so-called NSAIDs-exacerbated respiratory disease (NERD) [58]. Mast cells and eosinophils have roles in mediating many of the observed effects in NERD, including tissue infiltrates and mediator release such as prostaglandin 2 (PGD2) especially from mast cells. Increased levels of both IL-4 and interferon (IFN)-γ are present in the tissue of patients with NERD [59]: IL-4 is primarily responsible for the upregulation of leukotriene C4 (LTC4) by mast cells, while IFN-γ, but not IL-4, drives this process in eosinophils.
Effect of Eicosapentaenoic Acid on Body Composition and Inflammation Markers in Patients with Head and Neck Squamous Cell Cancer from a Public Hospital in Mexico
Published in Nutrition and Cancer, 2018
Obed Solís-Martínez, Valentina Plasa-Carvalho, Geraldine Phillips-Sixtos, Yanelly Trujillo-Cabrera, Arturo Hernández-Cuellar, Gloria E. Queipo-García, Eduardo Meaney-Mendiolea, Guillermo M. Ceballos-Reyes, Vanessa Fuchs-Tarlovsky
There is enough evidence to suggest that EPA contributes to normalize the pathophysiological alterations caused by anorexia-cachexia syndrome by quickly incorporating into the cell membranes which leads to metabolic control. The mechanism of action is still unknown, one hypothesis is that EPA competes with arachidonic acid (20:6 omega-6) in metabolic pathways involving the enzyme phospholipase A2 (cyclooxygenase and lipoxygenase), producing thromboxane's A3 (TXA3), leukotriene's B5 (LTB5), and prostaglandin's E3 (PGE3), metabolites which are less potent in inducing inflammation compared to the metabolites produced by arachidonic acid (thromboxane A2, prostaglandin E2, leukotriene B4, leukotriene C4, leukotriene D4) (13–18).