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Comparison of Healing Effect of DMSP in Green Sea Algae and Mesenchymal Stem Cells on Various Inflammatory Disorders
Published in Se-Kwon Kim, Marine Biochemistry, 2023
Furthermore, the transference of M1 macrophage to M2 macrophage which is caused by anti-inflammatory effects of AD-MSCs from rats promotes type 2 macrophage polarization to ameliorate the myocardial injury caused by diabetic cardiomyopathy (Jin et al., 2019). The polarization of type 2 macrophages appears to remarkably occur also by the administration of DMSP to Ehrlich Ascites Carcinoma (EAC), probably of mammary origin (Nakajima, 2015).
Nuclear Factor Kappa-B: Bridging Inflammation and Cancer
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Mohammad Aslam Khan, Girijesh Kumar Patel, Haseeb Zubair, Nikhil Tyagi, Shafquat Azim, Seema Singh, Aamir Ahmad, Ajay Pratap Singh
Transcriptional activation of NF-κB promotes gene expression associated with pro-inflammatory molecules such as chemokines, cytokines, matrix metalloproteinases (MMPs), adhesion molecules, cyclooxygenase-2 (cox-2), inducible nitric oxide (iNOS), etc. This inflammatory milieu activates and differentiates inflammatory T cells [4, 82]. These locally produced cytokines can activate macrophage and other monocyte lineage to execute and resolve inflammation. Furthermore, plasticity of immune cells gives rise to different subsets of polarized cells in response to the environmental signals, and underlying molecular mechanisms of macrophage polarization suggest the role of NF-κB signaling pathway. Moreover, NF-κB regulates the expression of pro-inflammatory molecules, such as IL-6, TNF-α, IL-1β, and Cox-2 in M1 macrophages [83]. Porta and colleagues reported that p50-NF-κB induces IL-10 expression (M2 marker), and mice deficient in p50-NF-κB exhibit M1-mediated inflammation [84]. In vivo study suggested that mice devoid of NF-κB signaling in T cells, exhibited delayed hypersensitivity responses and suppressed IFN-γ production [85]. NF-κB acts as a bridge between innate and the adaptive immune response by engaging components of adaptive arm of immunity. Furthermore, NF-κB-mediated cytokines (IL-12 and IL-23) trigger CD4+ T cell differentiation into T helper 1 (Th1) and Th17 [86, 87]. NF-κB has been implicated in many inflammation-associated diseases like type 2 diabetes, rheumatoid arthritis, atherosclerosis, multiple sclerosis, asthma, etc. [87, 88]
Mesenchymal Stem Cells from Dental Tissues
Published in Vincenzo Guarino, Marco Antonio Alvarez-Pérez, Current Advances in Oral and Craniofacial Tissue Engineering, 2020
Febe Carolina Vázquez Vázquez, Jael Adrián Vergara-Lope Núñez, Juan José Montesinos, Patricia González-Alva
When it comes to the immune response, macrophage polarization into M1 or M2 phenotype has often been at the origin of immunological paradigms. DPSCs transplantation on diabetic polyneuropathy, have found that the DPSCs stimulate macrophages polarization towards anti-inflammatory M2 phenotype, therefore, presenting immunosuppressive effects on diabetic polyneuropathy (Botelho et al. 2017).
Dysregulated metabolism: A friend-to-foe skewer of macrophages
Published in International Reviews of Immunology, 2023
Keywan Mortezaee, Jamal Majidpoor
Succinate induces production of pro-inflammatory IL-1β cytokine and hampers anti-inflammatory IL-1RA and IL-10 cytokines [15]. IL-10 released from M2 macrophages [64] favors OXPHOS metabolic predilection in such cells and hampers aerobic glycolysis in M1 macrophages [54]. Type II interferon, namely IFN-γ stimulates a fast rise in the rate of aerobic glycolysis in macrophages and their activation toward M1 macrophages. IFN-γ mediates IL-1β and nitric oxide (NO) generation through the respective HIF-1α [55, 65] and STAT1 pathways [55]. iNOS is a marker of M1 macrophages that is expressed at high levels in such cells [23]. IL-33 is another cytokine that acts for enhancing OXPHOS, and thereby promoting M2 polarization [12]. IL-33 is released from CAFs [44] and cancer cells [66] and activated eosinophils. The inducible effect of IL-4 on the scavenger receptor CD36 is contributed to the elevated OXPHOS and M2 activation through promoting the uptake and lipolysis of triacylglycerols [56]. IL-4 boosts the activity of protein kinase RNA-like ER kinase (PERK) for promoting M2 macrophage activation. Lipid oxidation and mitochondrial respiration, which are essential for M2 polarization, are hampered as a response to the PERK blockade [67]. IL-6/STAT3 is an inducer of M2 macrophage polarization [23, 68]. IL-6 level is seemingly co-related with higher lactate level [69]. The impact of ILs on macrophage metabolic rewiring is summarized in the Figure 1.
CLEC5a-directed bispecific antibody for effective cellular phagocytosis
Published in mAbs, 2022
Vivekananda Kedage, Diego Ellerman, Mingjian Fei, Wei-Ching Liang, Gu Zhang, Eric Cheng, Juan Zhang, Yongmei Chen, Haochu Huang, Wyne P. Lee, Yan Wu, Minhong Yan
A key requirement for the potential therapeutic use of CLEC5A-mediated phagocytosis is that tumor-associated macrophages (TAMs) express CLEC5A and respond to CLEC5A-engaging antibodies. As it has been widely reported that macrophages in different states of polarization express different sets of genes,27 we first characterized whether CLEC5A expression was specific for a specific type of polarization. We observed that, although with minor variations in mean fluorescence intensity, CLEC5A was expressed in macrophages polarized with different stimuli. This observation opened the possibility that the mechanism could be functional across different sets of macrophage subpopulations. Macrophage polarization is a continuum between fully M1 and M2 sites, with multiple factors present in the TME being capable of influencing the polarization state. As a result, macrophages present in the TME are usually a mixed population in different polarization states.28 In order to analyze macrophages in the context of TME, TAMs from two different tumor models, MC38 and CT26, were characterized and confirmed for their expression of CLEC5A, consistent with data from patients with ovarian cancer,29 osteosarcoma,30 and melanoma.31
β-Hydroxyisovalerylshikonin regulates macrophage polarization via the AMPK/Nrf2 pathway and ameliorates sepsis in mice
Published in Pharmaceutical Biology, 2022
Tao Pan, Yabin Chang, Min He, Zehui He, Jun Jiang, Xinling Ren, Fang Zhang
This study demonstrated for the first time that β-HIVS suppressed macrophage M1 polarization and promoted M2 polarization via activation of the AMPK/Nrf2 pathway. Macrophage is an attractive therapeutic target. The important role of macrophage polarization in the development of diseases has attracted considerable attention in recent years. Previous studies have shown that macrophage polarization is closely linked to autoimmune diseases, rheumatoid arthritis, and obesity (Wynn et al. 2013; Ma et al. 2019), and play a vital role in the progression of sepsis (Fu et al. 2020). The results of this study imply that β-HIVS may have therapeutic potential for the treatment of these diseases, especially sepsis, and its non‑cytotoxic dose is highly favourable to applied to clinical practice.