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Fundamental Aspects of Targeted Drug Delivery
Published in Neelesh Kumar Mehra, Keerti Jain, Dendrimers in Nanomedicine, 2021
Ameeduzzafar, Nabil K. Alruwaili, Md. Rizwanullah, Syed Sarim Imam, Muhammad Afzal, Khalid Saad Alharbi, Javed Ahmad
Complex diseases such as cancer or other inflammatory disorders are generally multifactorial in character, involving a severance of disease-mediating ligands and receptors. Some proinflammatory cytokines such as TNF, IL-1 and IL-6 have been recognized as key players in inflammatory diseases. In cancer, tumour cells often regulated diverse growth-promoting receptors that can act either independently or crosstalk intracellularly through signalling networks. Therefore, treatment with mAbs that target only a singular antigen has limitations and does not act on others (Dong et al. 2011). The barrier of multiple targets on one target should result in enhanced therapeutic efficacy. This can be achieved by combination therapy with mAbs but also other therapeutic compounds.
Overview of Immune Tolerance Strategies
Published in Richard K. Burt, Alberto M. Marmont, Stem Cell Therapy for Autoimmune Disease, 2019
Charles J. Hackett, Helen Quill
Treatment with anti-inflammatory cytokines provides an approach that extends beyond antigen specificity. Tissue inflammation and destruction in autoimmune diseases involves macrophages and other non antigen-specific cells54-56 which may be controlled by such counter-inflammatory cytokines as IL-10 and TGF-beta.57 Cytokine therapy requires achieving effective local concentrations, which risks severe side effects if delivered systemically. Local cytokine expression using gene therapy approaches are potential solutions to this problem, but such approaches are in early experimental stages.58 Novel methods, such as use of high affinity antibodies to block proinflammatory cytokines59 have great potential, but will require considerable early stage research. Enbrel, theTNF-alpha receptor approved for rheumatoid arthritis therapy, uses receptor blocking, an approach that appears more readily manipulated than directly affecting cytokine levels.60 Whether the ameliorating effects of cytokine circuit perturbation are strictly pharmacological or whether they may promote the development of tolerized cells or regulatory cell activation requires further investigation.
Active Targeting Strategies in Cancer with a Focus on Potential Nanotechnology Applications
Published in Mansoor M. Amiji, Nanotechnology for Cancer Therapy, 2006
Recognition of nanoparticles by TLR proteins may or may not act to stimulate potential target cells. If stimulation occurs, the result can include release of cytokines and a variety of potent regulatory molecules. Induction of pro-inflammatory cytokines may provide an undesirable outcome because cancerous states appear to be motivated by inflammatory events.53 The potential for a beneficial or negative impact of such outcomes would require case-by-case scrutiny. By themselves, nanoparticles have been shown to stimulate several cell-signaling pathways, including those that drive the release of pro-inflammatory cytokines such as interleukin (IL)-6 and IL-8.54,55 The incorporation of some therapeutic or diagnostic agents into nanoparticles can further enhance this potential for an inflammatory outcome.56 Additionally, a variety of nanoparticles, including fullerenes and quantum dots, has been shown to stimulate the creation of reactive oxygen species, and this effect can be enhanced by exposure to UV light that might be used for visualization and/or activation (reviewed in Oberdorster, Oberdorster, and Oberdorster57). As discussed at the beginning of this section, the potential for such events may be desirable for induction of selected events, e.g., immunization against cancer cell antigens. Nanoparticles can also be prepared to release cytokines that might affect an anti-tumor immune events event.58
A new Co(II)-bearing coordination polymer: structural characterization and treatment effect on CVB3-induced myocarditis via suppressing inflammatory response
Published in Inorganic and Nano-Metal Chemistry, 2020
Li-Jun Yu, Dong-Song Bai, Wen-Li Tang, Fu-Long Bi, Ming Zhao, Zhi-Hu Li
After infected with CVB3 virus, there was a significantly increased level of the predominant proinflammatory cytokines IL-1 and TNF-α produced by the damaged myocardium, which reflected the increased inflammatory response in cardiomyocytes. This increased inflammatory response would then promote monocyte activation and the further production of cytokines. So, in this experiment, the content of the proinflammatory cytokines in different groups was measured with ELISA. As results shown in Figure 4, the levels of IL-1 and TNF-α were much higher in the CVB3 model group than the normal group with significant difference (p < .05). However, in the CVB3 + compound group the production of proinflammatory cytokines was obviously reduced, almost back to the normal level. All these results indicated the compound could reduce the level of proinflammatory cytokines IL-1 and TNF-α in CVB3-induced myocarditis.
Evaluation of the proinflammatory effects of contaminated bathing water
Published in Journal of Toxicology and Environmental Health, Part A, 2019
Anas A. Sattar, Wondwossen Abate, Gyorgy Fejer, Graham Bradley, Simon K. Jackson
When LPS enters the bloodstream, even picogram amounts are capable of inducing a potent immunological reaction (Mayeux 1997; Rice et al. 2003; Velloso, Folli, and Saad 2015). In cells of the innate immune system, including monocytes and macrophages, LPS signals through the receptor TLR4 (Alexander and Rietschel 2001; Velloso, Folli, and Saad 2015) that initiates a signaling cascade leading to the release of various cellular mediators such as proinflammatory cytokines. Cytokines are small cell-signaling proteins that are released by various cells and they play a pivotal role in inflammation and the level of proinflammatory cytokines is generally elevated during inflammation (Lee and Lawrence 2018). Released cytokines act as messengers playing a key role in regulating and initiating inflammatory responses to LPS which is augmented by attracting more immune cells to the affected site (Groves and Jiang 1995; Lee and Lawrence 2018; Masi et al. 2017). In extreme cases, excessive induction of proinflammatory cytokines by LPS results in septic shock, organ failure and death (Shapira et al. 1996). In the lung, alveolar macrophages also respond to LPS via TLR4 recognition which was linked to asthma-like conditions and lung injury (Helyes and Hajna 2012).
Association between prenatal period exposure to ambient air pollutants and development of postpartum depression: a systematic review and meta-analysis
Published in International Journal of Environmental Health Research, 2022
Seyedeh Azam Pourhoseini, Ali Akbary, Hedieh Mahmoudi, Maryam Akbari, Seyed Taghi Heydari
Finding estimated in this study regarding exposure to PM10 is generally in line with recently published systematic review and meta-analysis on being exposed to air pollution and developing depressive disorders (Borroni et al. 2022). The review included 39 observational studies and showed that there were statistically significantly increased odds of development of depression following less than one month exposure to components such as PM10.Besides, consistently, no relationship was observed between exposure to O3 and depression. This relationship between exposure to ambient air pollution and development of disorders of central nervous system such as depression has also been reported in animal studies (Calderón-Garcidueñas et al. 2002, 2004; Liu et al. 2018; Ehsanifar et al. 2022). In an experimental study, BALB/c male mice were recruited and then divided to receive either filtered air, control group, or concentrated ambient matters (Campbell et al. 2005). The study showed that there were significantly higher levels of proinflammatory cytokines including interleukin-1 alpha and tumor necrosis factor alpha. Similar finding was observed in dogs lived in areas with high concentration of PM10 compared with those in less polluted regions (Calderón-Garcidueñas et al. 2002). With this body of evidence regarding the association of air pollutants exposure and depressive disorder, the relationship between ambient air pollution and PPD could be completely expected. However, we could not find significant associations between the other PM, PM2.5, and development of PPD. Besides, studies have shown that the women are more prone to psychiatric disorders in their gestation and puerperium which may lead to an increased risk of PPD (Cantwell et al. 2006; Koman et al. 2018).