Physiology of veins and lymphatics
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland in Manual of Venous and Lymphatic Diseases, 2017
Cytokines are either antior pro-inflammatory. Anti-inflammatory cytokines promote healing and reduce inflammation, whereas pro-inflammatory cytokines, though necessary for healing, generally make disease worse and can cause auto-immune conditions.Anti-inflammator y cytokines that regulate this response include interleukin (IL)-1 receptor antagonist, IL-4, IL-10, IL-11, and IL-13.Pro-inflammatory cytokines include interleukins (IL-1β, IL-6) and tumour necrosis factor (TNF-α). IL-1β is released primarily by monocytes, macrophages, fibroblasts and endothelial cells during cell injury, infection and inflammation. Once released, they induce a cascade of further cytokine production.Various cytokines termed chemokines induce activation and migration of leukocytes. They include monocyte che-moattractant protein (MCP-1), monocyte inflammatory protein (MIP-1α, MIP-1β) and growth related oncogene (GRO/KC).
Subfamily Bombacoideae
Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa in Wild Plants, 2020
Cytokines are regulators of the human body, and react to infection, trauma, immune responses, and inflammation. Some cytokines act to increase the body’s reaction to inflammatory stimulus, making it worse (pro-inflammatory), while others help to decrease inflammation, and induce the healing process (anti-inflammatory). The major pro-inflammatory cytokines include Interleukin-1alpha (IL-1α), IL1-beta (IL-1 β), IL-6, and TNF-alpha (TNFα). Inhibiting the expression of these pro-inflammatory cytokines has been demonstrated as the mechanism of action of many anti-inflammatory medicinal plants and their isolated compounds (Dinarello 2000). Conducting a comparative study on cytokine modulatory activities of different sources of Adansonia digitata, the aqueous, methanol, and DMSO extracts of commercial products of A. digitata leaves, fruits, and seeds were evaluated for their ability to secrete cytokine (IL-6 and ILr-8) in human epithelial cell cultures. Many of the extracts, especially leaf extracts, proved to be active as cytokine modulators, some of which were pro-inflammatory, and others anti-inflammatory. The overall results concluded the presence of multiple bioactive compounds in different parts of the plant, explaining the variable medical benefits in the treatment of infectious diseases and inflammatory conditions among the three plant sources (Selvarani and Hudson 2009).
Treating the Underlying Causes of Synovitis, Degenerative Joint Disease and Osteoarthritis in Primary Care
Kohlstadt Ingrid, Cintron Kenneth in Metabolic Therapies in Orthopedics, Second Edition, 2018
An abridged explanation of the inflammatory and reparative responses in osteoarthritis is depicted in Figure 24.1. There are at least 19 cytokine factors as well as growth factors involved in the pathogenesis and repair of joints [32]. The major pro-inflammatory cytokines are IL-1ß, IL-6, IL-15, IL-17, IL-18 and tumor necrosis factor alpha (TNF-α). The collagenase matrix metalloproteinase-13 (MMP-13) is the principal collagen-II-degrading enzyme in articular cartilage. Aggrecanases are the principal aggrecan-degrading enzymes. When these proteinases are activated, the destruction of articular cartilage progresses rapidly. The anti-inflammatory cytokines are IL-4, IL-10 and IL-13. The problem arises when the catabolic/inflammatory processes surpass the matrix anabolic/synthetic activities leading to the progressive destruction of the articular cartilage in osteoarthritic joints [33].
Serum calprotectin correlates with risk and disease severity of ankylosing spondylitis and its change during first month might predict favorable response to treatment
Published in Modern Rheumatology, 2019
Hua Hu, Fei Du, Shizhan Zhang, Weiguo Zhang
Inflammatory cytokines are a class of chemicals excreted by leukocytes and some non-immune cells such as epithelial cells, released into the inflammation cites and function as pro-inflammatory or anti-inflammatory factors [27]. The results in our study characterized that baseline calprotectin level in serum was positively associated with expressions of IL-1β, IL-17 and TNF-α in AS patients. It has been reported that the production of calprotectin by monocytes, which is correlated with the activation of DNA C/EBP alpha binding complex, can be promoted by Porphyromonas gingivalis (P-LPS), TNF-α and IL-1β [28]. And in a mouse model, calprotectin is involved the up-regulation of interleukin (IL)-17 [24]. Those mechanisms discovered by previous studies might explain the correlations of calprotectin with IL-1β, IL-17 and TNF-α in our study. Clinical studies have reported positive correlations of calprotectin with the expressions of other inflammatory cytokines, too. Serum calprotectin was positively associated with the levels of IL-2, IL-6 and interferon-γ in patients with sepsis in the intensive care unit [29].
Potential biomarkers for predicting hemorrhagic transformation of ischemic stroke
Published in International Journal of Neuroscience, 2018
Guanfeng Lu, Quanwei He, Yan Shen, Fei Cao
Higher levels of high-sensitivity C reactive protein (hsCRP), a marker of inflammation, have been shown to be a prognostic indicator in patients, especially those with acute cardioembolic stroke [35,36]. A study showed that hsCRP values tended to be higher in acute cardioembolic stroke with sICH, and the sensitivity and specificity were 64% and 69%, respectively with a cut-off value of 9.0 mg/L, but hsCRP was not an independent predictor in logistic regression analysis [37]. Vascular adhesion protein-1 (VAP-1) is a cell surface and circulating enzyme involved in recruitment of lymphocytes and neutrophils through its semicarbazide-sensitive amine oxidase (SSAO) activity. Baseline VAP-1/SSAO activity predicted PH in patients with ischemic stroke after t-PA administration, and anti-VAP-1/SSAO drugs given with t-PA prevented neurological worsening in a rat model [38]. Inflammatory cytokines play an important role in mediating a cascade of biological activities. Tumor necrosis factor-α (TNF-α) can induce MMP-9 production, promoting HT [21,39]. Furthermore, TNF-α, interleukin-1 (IL-1) and other cytokines can activate MMP-3, which converts proMMP-9 into active MMP-9 [1]. IL-6 has been demonstrated to be significantly higher whereas IL-10 was lower in patients with HT [40]. Pre- and post-t-PA variation of IL-10 was a significant predictor of sICH in patients with ischemic stroke [41]. These findings suggest that inflammatory cytokines may be possible predictive factors for HT.
Effect of biological DMARDs and JAK inhibitors in pain of chronic inflammatory arthritis
Published in Expert Opinion on Biological Therapy, 2022
Alessandra Alciati, Marco Di Carlo, Cesare Siragusano, Antonino Palumbo, Ignazio Francesco Masala, Fabiola Atzeni
Traditionally, pain in IA was ascribed to peripheral joint inflammation. Although the etiology of IA is still unknown, the altered activation of the immune system, through hyper-expression of pro-inflammatory cytokines, plays a central role in joint involvement [3]. During the inflammatory process, both pro- and anti-inflammatory cytokines are released. Amongst the pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) act on cytokine receptors placed on the nociceptors, activating second messenger systems, modifying excitability and ionic currents, and regulating molecules involved in nociception. Thus, cytokines can contribute to pain both directly, by acting on nociceptive neurons, and indirectly, by inducing the release of other mediators acting on neurons as well, such as the prostaglandins, which in turn increase neuron sensitivity [4,5].
Related Knowledge Centers
- Inflammation
- Interferon Gamma
- Interleukin 12
- Interleukin 18
- Interleukin 6
- T Helper Cell
- Tumor Necrosis Factor
- Cytokine
- Macrophage
- Interleukin-1 Family