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Cytokine Effects on Extracellular Matrix
Published in Jason Kelley, Cytokines of the Lung, 2022
Ganesh Raghu, Michael Kinsella
Definitive evidence for the physiological and pathological actions of a cytokine requires studies in intact organisms and tissues. Continued investigations of local expression of specific cytokine(s), effect of cytokine(s), and cytokine-cytokine interactions in the context of homotypic and heterotypic cellular interactions, and colocalization of ECM components with specific cytokine(s) in morphogenesis and disease models of lung injury and repair are needed. Studies to associate natural or induced states of cytokine excess with therapeutic or pathological effects, and their correction by depletion will undoubtedly offer important insights. Investigations to block specific cytokine action on abnormal ECM deposition may lead to future therapies. In vitro and in vivo studies to determine cytokine effects have their own merits and disadvantages. The importance of cell–cell communication has been stressed during the past several years as a key to understanding biological functions of cells and their extracellular milieu in the complex context of cytokine effects. Studies in long-term lung organ cultures may offer a compromised model between in vitro and in vivo conditions to study the effects of a specific cytokine on ECM in pulmonary tissue.
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
The levels of IL-2, IL-7, IL-10, GSCF, IP-10, MCP1, MIP1a, and TNF-α in the blood of severely ill COVID-19 patients were also elevated. In short, the aberrant release of multiple cytokines appears to trigger a cytokine storm that produces immunopathogenic damage to tissues and organs, even while the immune response seeks to suppress and eradicate the virus (Wiersinga et al., 2020). Thus, it can be mentioned that the cytokine storm involves an immune response that causes collateral damage that may be greater than the immediate benefit of the immune response. Figure 7.5 and Table 7.1 represent specific organs involved and respective signs and symptoms of a systemic cytokine storm. Further studies should be done to find out the detailed pathogenesis of COVID-19 and cytokine storms (Wiersinga et al., 2020; Price et al., 2020; Dutta et al., 2020; Fajgenbaum and June, 2020; WHO, 2020a; Yuki et al., 2020; Kumar and Al Khodor, 2020; Parasher, 2021; Cevik et al., 2020; Abbas et al., 2016; Oliveira et al, 2020).
Anaphylaxis
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
IgG-mediated anaphylaxis has been demonstrated in mouse models and is postulated to be involved in anaphylaxis in humans to omalizumab or other monoclonal antibodies (Cox et al. 2007, Cheifetz et al. 2003). Immune complex/complement-mediated mechanisms may be involved in reactions to protamine and some other drugs. In reactions to Radio Contrast Media (RCM), RCM molecules may interact with the Fc portion of IgE or IgG already bound to mast cells or basophils, directly causing cross-linking and cell activation (Brockow and Ring 2011). Cytokine storm-like reactions, characterized by chills and fever, followed by hypotension, desaturation and cardiovascular collapse can occur with chimeric, humanized and human monoclonal antibodies and chemotherapy. Cytokine storm reactions are systemic inflammatory responses instigated by leukocyte release of pro-inflammatory cytokines (TNF-α, IL-1B, and IL-6) (Castells 2017).
Pharmacotherapeutic options for cancer cachexia: emerging drugs and recent approvals
Published in Expert Opinion on Pharmacotherapy, 2023
Lorena Garcia-Castillo, Giacomo Rubini, Paola Costelli
Anti-cytokine strategies are based on the blockade of a cytokine synthesis or action. Relevant examples are etanercept, infliximab, pentoxifylline, and thalidomide. Pentoxifylline, an agent reducing blood viscosity, etanercept, and infliximab, both anti-TNF-α monoclonal antibodies, have been studied as TNF-α targeting agents, showing that no improvement of cachexia could be observed in cancer patients [33,35]. Thalidomide is a glutamic acid derivative able to suppress several cytokines (including TNF-α and IL-6) and to inhibit NF-kB, thereby exerting, among others, an anti-inflammatory effect. Patients treated for four weeks with thalidomide gained 0.37 kg of body weight and 1.0 cm3 in arm muscle mass, while the placebo group lost 2.21 kg and 4.6 cm3, respectively [33]. The most promising results came from a phase II study in which non-small cell lung cancer patients administered a humanized anti-IL6 antibody showed improvement of anemia and cachexia [36]. Consistently, tocilizumab, an anti-IL6 receptor antibody was reported to effectively counteract cachexia. However, nowadays no anti-IL6 strategy reached the approval for clinical use.
Local delivery of interleukin 7 with an oncolytic adenovirus activates tumor-infiltrating lymphocytes and causes tumor regression
Published in OncoImmunology, 2022
Tatiana V. Kudling, James H.A. Clubb, Dafne C.A. Quixabeira, Joao M. Santos, Riikka Havunen, Alexander Kononov, Camilla Heiniö, Victor Cervera-Carrascon, Santeri Pakola, Saru Basnet, Susanna Grönberg-Vähä-Koskela, Victor Arias, Ivan Gladwyn-Ng, Katri Aro, Leif Bäck, Jari Räsänen, Ilkka Ilonen, Kristian Borenius, Mikko Räsänen, Otto Hemminki, Antti Rannikko, Anna Kanerva, Johanna Tapper, Akseli Hemminki
Cytokines are small protein molecules that provide growth, differentiation, and inflammatory or anti-inflammatory signals to different cell types. Cytokine immunotherapy is an appealing approach for treating cancer patients with advanced malignancies because signals transduced via cytokines activate the host immune system, making it more efficient in the recognition and elimination of cancer cells. However, to date, only two cytokines – interleukin 2 (IL2) and interferon-alpha – are approved by the U.S. Food and Drug Administration for cancer treatment.1,2 Both of them can stimulate the proliferation and activation of T cells, but high concentrations are needed to achieve therapeutic efficacy in cancer patients. Consequently, increasing the systemic dose results in adverse events before sufficient tumor concentrations can be reached.3–5
Prevention of ulcerative colitis by Huangqin decoction: reducing the intestinal epithelial cell apoptosis rate through the IFN-γ/JAK/ETS signalling pathway
Published in Pharmaceutical Biology, 2022
Xiaowei Mo, Kairui Tang, Lijing Deng, Xingyi Zhou, Xiaojuan Li, Yupei Zhang, Jing Wang
In the pathogenesis of UC, there are not only abnormalities in the local immune function of the intestinal mucosa but also systemic immune disorders. Cytokines are involved in the immune response and inflammatory process. To evaluate the overall proinflammatory and anti-inflammatory systems in mice, we assessed levels of proinflammatory cytokines (IL-8, TNF-α, IL-17 and IFN-γ) and anti-inflammatory cytokines (TGF-β, IL-4 and IL-10) in the serum (Figure 3). The results showed that whether pro-inflammatory cytokines or anti-inflammatory cytokines were present, the levels of these cytokines in the UC group were significantly higher than those in the NC group. This result suggests that the host may trigger proinflammatory and anti-inflammatory systems during the pathogenesis of acute UC, resulting in increased inflammatory cytokines. After treatment, serum levels of IL-8, TNF-α, IL-17, IFN-γ, TGF-β, IL-4 and IL-10 in the UC + HQD group were significantly lower than those in the UC group, indicating that HQD improved the immune function of the host system, regulated the proinflammatory and anti-inflammatory systems, and reduced inflammatory damage in model mice.