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Orbital Inflammatory Syndromes
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Jaspreet Sukhija, Savleen Kaur
The orbital and periorbital tissues are quiet susceptible to inflammation from many conditions. The most commonly studied mechanism is immune-related idiopathic orbital inflammations. Co-occurrence of certain rheumatological disorders such as Wegener's granulomatosis, sarcoidosis, giant cell arteritis, SLE, dermatomyositis, and rheumatoid arthritis further indicate that it is an autoimmune disease. Specific circulating antibodies have not been yet found associated with the condition. Inflammatory cytokines such as interleukin-1 are known to be increased. Immunohistochemical staining of tissue samples demonstrates the presence of toll-like receptors suggesting an abnormal innate immune response may be responsible.
Natural Products in the Treatment of Unremitting Wounds Secondary to Diabetes or Peripheral Vascular Disease
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
In a normal wound healing process, inflammation begins quickly and lasts approximately 3–7 days, during which time neutrophils, macrophages and lymphocytes work toward phagocytosis, releasing growth factors and cytokines, and initiating pro-inflammatory conditions. As seen in people with poorly controlled diabetes, dysfunction arises in this phase, as well, initially with a decreased number of neutrophils limiting phagocytosis (Baltzis, Eleftheriadou, and Veves, 2014). In hyperglycemic conditions, studies have shown a decrease in leukocyte adherence, chemotaxis and the production of growth factors (Oguntibeju, 2019). Once inflammatory cells are present, an increase in pro-inflammatory cytokines can contribute to a prolonged inflammatory response and chronic inflammation (Patel, Srivastava, Singh, and Singh, 2019).
Psychosocial Aspects of Diabetes
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
There are no common genetic factors that explain the association between depression and diabetes. However, there is a definite pathophysiological cycle between diabetes and depression. This is based on activation and disturbance of the body’s stress system. Chronic stress activates the hypothalamus-pituitary-adrenal axis and the sympathetic nervous system. This increases production of cortisol in the adrenal cortex, plus the production of adrenaline and noradrenaline in the adrenal medulla. Chronic hypercortisolemia promotes insulin resistance as well as visceral obesity, leading to metabolic syndrome and type 2 diabetes. Chronic stress and related hormones activate the fear system and the reward system – producing depression and cravings for food. Chronic stress also induces immune dysfunction, resulting in increased production of inflammatory cytokines. In large amounts, the cytokines interact with function of the pancreatic beta cells, leading to insulin resistance and type 2 diabetes. Inflammatory responses are also involved in the pathophysiology of depression. Therefore, stress and inflammation promote both depression and diabetes.
Resveratrol Attenuates Ankylosing Spondylitis in Mice by Inhibiting the TLR4/NF-κB/NLRP3 Pathway and Regulating Gut Microbiota
Published in Immunological Investigations, 2023
Ming-Hui Ding, Peng-Gang Xu, Ying Wang, Bao-di Ren, Jun-Li Zhang
Some strong evidence confirmed that inflammatory cytokines were important factors affecting chronic inflammatory diseases and targets for disease therapy (Baeten et al. 2015). To assess the effect of RES on inflammation in AS mice, we examined the expression levels of pro- and anti-inflammatory cytokines in circulating blood. The outcomes indicated that, compared with the CTRL group, serum levels of pro-inflammatory cytokines TNF-α, IL-6, IL-17A and IFN-γ were significantly increased while levels of anti-inflammatory cytokine IL-4 were significantly decreased in the AS group. RES (20 mg/kg and 50 mg/kg) treatment could achieve a notable decline in TNF-α, IL-6, IL-17A and IFN-γ expression and a marked rise in IL-4 expression (p < .05, Figure 2(a–e)). In a word, RES treatment decreased the expression of pro-inflammatory cytokines and increased the expression of anti-inflammatory cytokines in AS mice.
The effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on ischemic stroke and the possible underlying mechanisms
Published in International Journal of Neuroscience, 2023
Yuxia Song, Hongyang Fan, XiaoJia Tang, Yuhan Luo, Peipei Liu, Yingzhu Chen
In addition, the adaptive immunity of the patient also plays an important role in antiviral activity. Depletion of CD4+ T cells is associated with reduced recruitment of lymphocytes in the lungs and reduced production of neutralizing antibodies and cytokines, leading to strong immune-mediated interstitial pneumonia and delayed viral clearance from the lungs [17]. T helper cells produce pro-inflammatory cytokines through the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signaling pathway [18]. Interleukin (IL)-17 recruits monocytes and neutrophils to sites of infection and activates downstream cytokine and chemokine cascades producing IL-1, IL-6, IL-8, IL-21, tumor necrosis factor (TNF)-β, and monocyte chemoattractant protein-1 (MCP-1) [19]. C3a and C5a have strong pro-inflammatory effects, which can stimulate the recruitment of inflammatory cells and the activation of neutrophils [7]. The key to the pathogenesis of COVID-19 is related to the reduction of innate immune response-related antiviral effects and the increase in the production of inflammatory cytokines. The increase of inflammatory cytokines is related to a more serious prognosis [20].
Molecular and epigenetic modes of Fumonisin B1 mediated toxicity and carcinogenesis and detoxification strategies
Published in Critical Reviews in Toxicology, 2021
Thilona Arumugam, Terisha Ghazi, Anil A. Chuturgoon
Inflammation is a non-specific response that acts by removing harmful stimuli and initiating repair through the activation of phagocytes. The activated phagocytes secrete cytokines that act as chemical messengers between other immune cells (Oswald et al. 2005). They stimulate or inhibit the growth and activity of various immune cells, which mediate and regulate immunity and inflammation. Proinflammatory cytokines mediate inflammation via receptor activation, which can trigger intracellular signalling pathways such as MAPK, nuclear factor kappa B (NFκB), and Janus kinase/signal transducer and activator of transcription (JAK/STAT). While inflammation plays an important role in immune response, excessive production of inflammatory cytokines can lead to cytotoxicity and tissue damage (Chen, Mitchell et al. 2018).