China
Africa
Explore chapters and articles related to this topic
Immuno-Pathologic Basis of COVID-19 and the Management of Mild and Moderate Cases
Published in Srijan Goswami, Chiranjeeb Dey, COVID-19 and SARS-CoV-2, 2022
Debdeep Dasgupta, Srijan Goswami, Chiranjeeb Dey
In immunocompetent individuals, SARS-CoV-2 infection leads to hypercytokinemia, an unregulated hyperinflammatory response that results from the systemic spread of a localized inflammatory response to viral or bacterial infection. Increased proliferation, differentiation, and activation of T-lymphocytes, NK-cells, macrophages, elevated secretion of pro-inflammatory cytokines, and chemokines are indicative of a potentially fatal condition, the cytokine storm. In the initial stages of hypercytokinemia, the rise in the concentration of tumor necrosis factor and interleukin-1β (acute response cytokines) and interleukin-8 and monocyte chemoattractant protein-1 (chemotactic cytokines) leads to an increase in the concentration of interleukin-6 (IL-6). Interleukin-6 promotes inflammatory processes by binding to membrane-bound or soluble IL-6 receptors (mIL-6R [cis-signaling] or sIL-6R [trans-signaling]), creating interaction with glycoprotein-130 (gp-130) and through the JAK-STAT pathway regulates the concentration of IL-6, MCP-1, and GM-CSF. The serum concentration of ferritin, complement, C-reactive protein, and coagulation factors are increased due to the acute phase reaction triggered by IL-6 and associated inflammatory mediators. The reduction in the rate of viral clearance during this stage is related to a decrease in cytotoxic T lymphocyte count, a decrease in total lymphocyte count, and an abnormal rise in serum cytokine levels induced by IL-6. Leakage from blood vessels and complement and coagulation pathway activation caused by IL-6 may lead to severe cytokine release syndrome (CRS) or diffuse intravascular coagulation (DIC). An increased level of IL-6 may cause cardiac dysfunction, endothelial dysfunction, hypotension, and blood clotting disorders (Price et al., 2020; Weirsinga et al., 2020; Fajgenbaum and June, 2020) (Figure 7.3).
Interaction of bone and brain: osteocalcin and cognition
Published in International Journal of Neuroscience, 2021
Misa Nakamura, Masakazu Imaoka, Masatoshi Takeda
Glucose and fatty acid uptake and consumption during exercise are crucial factors in neuropathological change and cognition. Mera et al. reported that circulating OC levels were doubled during aerobic exercise in mice, and that OC signaling in myofibers was necessary for the adaptation to exercise by increasing glucose and fatty acid uptake and catabolism. OC signaling also contributes significantly to the exercise-induced release of interleukin-6 (IL-6), a myokine from myofibers that promotes adaptation to exercise by increasing the production of bioactive OC [41]. IL-6 is known to regulate energy and glucose homeostasis and to increase energy sensitivity in obese mice through glycoprotein 130 (gp130) [67]. Gp130 in osteocytes regulates OC gene expression in osteoblasts [68]. In addition, exogenous OC has been shown to enhance the physical ability of young mice and to restore the physical ability of 15-month-old mice to that of 3-month-old mice [41]. These findings indicate that OC signaling in myofibers improves energy homeostasis and cognition through the exercise-induced activation of the IL-6/gp130/OC axis [41].
Interleukin-11 Overexpression and M2 Macrophage Density are Associated with Angiogenic Activity in Proliferative Diabetic Retinopathy
Published in Ocular Immunology and Inflammation, 2020
Ahmed M. Abu El-Asrar, Ajmal Ahmad, Eef Allegaert, Mohammad Mairaj Siddiquei, Priscilla W. Gikandi, Gert De Hertogh, Ghislain Opdenakker
Interleukin-11 (IL-11) is a multifunctional member of the IL-6 family of cytokines which include cytokines that share the use of the glycoprotein-130 (gp130) receptor β-subunit signaling pathway. The engagement of the gp130 receptor induces the activation of the Janus kinase (JAK)/signal transducer and activator of transcription 3 (STAT3) pathway.11,12 Signaling by IL-11 proceeds via an interaction of the protein with its membrane-specific receptor IL-11Rα and a subsequent interaction of the complex with the transmembrane signal-transducing receptor gp130.13 IL-11 has been strongly implicated as a proinflammatory and proangiogenic cytokine in the pathogenesis of various inflammation-associated cancers of epithelial cell origin14–18 as well as in autoimmune and inflammatory diseases.19–21
Emerging roles for Interleukin-11 in disease
Published in Growth Factors, 2019
Paul M. Nguyen, Suad M. Abdirahman, Tracy L. Putoczki
The interleukin (IL)-6 family of cytokines consists of IL-6, IL-11, leukemia inhibitory factor (LIF), Oncostatin M (OSM), ciliary neurotrophic factor (CNTF), cardiotrophin 1 (CT-1), cardiotrophin-like cytokine (CLC), IL-27, and IL-31. Members of this family were grouped together, in part, due to their shared use of the ubiquitously expressed type I cytokine receptor glycoprotein 130 (GP130) for signal transduction. However, unlike the other family members, IL-6 and IL-11 are similar in that they both signal through a hexameric complex formed by the cytokine, specific cytokine receptor (IL-6R or IL-11R), and GP130 (Barton et al. 2000; Boulanger et al. 2003). Discovered over 30 years ago (Hirano et al. 1986), roles for IL-6 in disease have dominated the literature, with our understanding of the remaining family members still in their infancy. This review will provide an overview of recent advances in IL-11 biology.