China
Africa
Explore chapters and articles related to this topic
Infiltrative Optic Neuropathies
Published in Vivek Lal, A Clinical Approach to Neuro-Ophthalmic Disorders, 2023
Aniruddha Agarwal, Sabia Handa, Vishali Gupta
Treatment of sarcoidosis in general and neurosarcoidosis, in particular, may be extremely difficult. Corticosteroids are the mainstay of therapy; there are no standardized treatment protocols available as yet. Although corticosteroids are very effective in controlling inflammation initially, their long-term use is often associated with significant complications.70,71 Among patients where chronic steroid usage (≥7.5 mg of prednisone or equivalent daily) is required to control the inflammation, the use of steroid-sparing agents is indicated. Immunosuppressive agents such as hydroxychloroquine, methotrexate, azathioprine, mycophenolate mofetil, or cyclosporine may be useful. Rarely, patients may require biological agents including antagonists of tumor necrosis factor (TNF) such as adalimumab, infliximab or etanercept.75,76
Tumor Necrosis Factor
Published in Jason Kelley, Cytokines of the Lung, 2022
Tumor necrosis factor is a multifunctional cytokine, the in vivo biological effects of which are a combination of direct effects on target cells possessing specific TNF receptors and indirect effects that are mediated by a multitude of TNF-induced secondary cytokines and other inflammatory mediators. The TNF protein is not usually thought to be constitutively expressed under physiological conditions, although a role for TNF has been postulated during physiological tissue remodeling (Tracey et al., 1989). TNF is generally considered to be a proinflammatory cytokine that acts together with interleukin-1 (IL-1) to orchestrate local inflammation when present at relatively low concentrations in localized tissue compartments, such as the lung. Usually, both TNF and IL-1 are probably up-regulated in concert in vivo. TNF and IL-1 each individually can lead to hypotension and hemorrhagic shock at higher systemic concentrations (Tracey et al., 1986; Okusawa et al., 1988), as occurs, for example, after their experimental intravenous administration or as might occur when systemic sepsis develops in a patient with a pulmonary infection. TNF levels rise rapidly in the serum of rodents (Waage, 1987; Ulich et al., 1990a) and primates (Fong et al., 1989) after the intravenous injection of lipopolysaccharide (LPS) or gram-negative bacteria, and antiserum to TNF can inhibit LPS- or bacteria-induced lethal shock (Beutler et al., 1985b). TNF can act synergistically with IL-1 to induce acute neutrophilic inflammation (Wankowicz et al., 1988), as well as lethal shock (Waage and Espevic, 1988).
The Great Influenza
Published in Rae-Ellen W. Kavey, Allison B. Kavey, Viral Pandemics, 2020
Rae-Ellen W. Kavey, Allison B. Kavey
The symptoms of influenza reflect a combination of direct effects of the virus on respiratory epithelial cells and systemic symptoms from the elaboration of cytokines, cell signaling molecules that aid cell-to-cell communication in immune responses and stimulate the movement of cells towards sites of infection. Following primary exposure, cytokine inflammatory responses are triggered when infected cells die, increasing blood flow, and bringing plasma and leukocytes (white blood cells) to the site of injury, elevating local temperatures, and causing pain. The acute inflammatory response is also marked by the activation of pro-inflammatory cytokines including interleukin-6 (IL-6), type 1 interferons, and tumor necrosis factors (TNFs) like TNF-alpha; a combination of these factors is considered to be responsible for the respiratory tract symptoms of pain, congestion and cough plus systemic symptoms of fever, muscle pain, headache and exhaustion. Increasing inflammation is accompanied by immune cell infiltration and tissue damage. As the infection subsides, the epithelium is regenerated; in most cases, function can be completely restored by this reparative process.6
Ameliorative effect of chitosan nanoparticles against carbon tetrachloride-induced nephrotoxicity in Wistar rats
Published in Pharmaceutical Biology, 2022
Yousra A. Nomier, Saeed Alshahrani, Mahmoud Elsabahy, Gihan F. Asaad, Azza Hassan, Walaa A. El-Dakroury
Carbon tetrachloride (CCl4) is an organic compound widely used in the manufacturing of cleaning agents and solvents, and in the synthesis of chlorofluorocarbons (Unsal et al. 2021). However, CCl4-induced nephrotoxicity may be due to oxidative stress and free radicals which is mediated by cytochrome P450 located in the renal proximal tubules (Ronis et al. 1998). Proinflammatory cytokines possess a pivotal role in inflammation and immunity as well as cellular proliferation, migration, and adhesion. Interleukins and tumour necrosis factors are involved in the upregulation of inflammatory responses (Hamid et al. 2017). CCl4 was also implicated in cell apoptosis which leads to various alterations in cellular morphology such as cell shrinkage, DNA fragmentation, and mRNA decay (Safhi 2018). Cellular apoptosis is initiated by the activation of caspase 9 (initiator caspase) followed by the activation of caspase 3 (executioner caspase) causing cellular death due to protein degradation (Rudel 1999).
Efficacy and safety of adalimumab in Japanese patients with psoriatic arthritis and inadequate response to non-steroidal anti-inflammatory drugs (NSAIDs): A prospective, observational study
Published in Modern Rheumatology, 2020
Akimichi Morita, Ryuhei Okuyama, Norito Katoh, Chiharu Tateishi, Koji Masuda, Toshifumi Komori, Eisaku Ogawa, Takamitsu Makino, Emi Nishida, Shohei Nishimoto, Kenzo Muramoto, Daisuke Tsuruta, Hironobu Ihn
Tumor necrosis factor-α (TNF-α) is pivotal to the chronic inflammation and aberrant immune responses associated with rheumatoid arthritis (RA), psoriasis, and PsA, and is present in higher concentrations in the joints and skin of patients with PsA than those without [8,9]. In addition to the aforementioned genotypic differences, population differences exist with regard to an association between TNF-α gene polymorphisms and PsA; for example, an association was not found in Japanese studies but was observed, especially with regard to joint erosion in early PsA, in studies involving Caucasians [10]. Biologic agents that inhibit TNF-α (e.g. etanercept, infliximab, and adalimumab) are efficacious in the treatment of RA, psoriasis, and PsA either as monotherapy or in combination with methotrexate [1,2,11–16]. In a study in a clinic setting, methotrexate was associated with a significant increase in radiographic damage compared to TNF-α blockers in patients with erosive PsA [17]. Moreover, according to the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis 2015 treatment recommendations for PsA, TNF-α inhibitors are strongly recommended in patients with inadequate response to DMARDs or other biologics, regardless of clinical manifestation (peripheral PsA, axial PsA, enthesitis, dactylitis, psoriasis, and nail psoriasis) [18].
Associations between IL-23R gene polymorphisms and the susceptibility of rheumatoid arthritis: a meta-analysis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Qinghua Zou, Yi Zhao, Yong Wang, Yongfei Fang, Yi Liu
The pathogenesis of RA is still not completely understood, with an average prevalence rate of approximately 1% worldwide, and there are around 4 million RA patients in China. No specific medicine has been developed for the therapy of RA so far. Since conventional therapeutic approaches can only relieve patients’ pains and inflammations, retard or terminate the damages of joints, improve the health degree and action competence, they cannot radically cure such disease fundamentally. In recent years, the unceasing development of molecular biology has revealed that the mediation of cytokines may have pivotal influences on the generation and growth of joint diseases. The functions of cytokines such as interleukin and tumour necrosis factors are the critical mechanism of inflammatory responses.