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Macrophage Targeting: A Promising Strategy for Delivery of Chemotherapeutics in Leishmaniasis and Other Visceral Diseases
Published in Sarwar Beg, Mahfoozur Rahman, Md. Abul Barkat, Farhan J. Ahmad, Nanomedicine for the Treatment of Disease, 2019
Jaya Gopal Meher, Pankaj K. Singh, Yuvraj Singh, Mohini Chaurasia, Anita Singh, Manish K. Chourasia
Liver is a vital organ of body that regulates many physiological functions and maintains homeostasis. Diseases in liver are caused by chemical or biological insults, pathogens, or even mechanical injury. In case of liver injury, activation of immune cells like kupffer cells occurs, leading to secretion of inflammatory mediators that increase cytotoxicity and chemotaxis. So kupffer cells, local residents in liver are a major player in hepatocellular destruction. At the same time these immune cells are also known for their protective action mediated via production of IL–10 and IL–18. Fatty liver is another major concern in liver-related complications which may be either alcoholic or non-alcoholic fatty liver. In both cases, progression leads to hepatic steatosis and steatohepatitis which results in cirrhosis and liver cancer. As these are chronic inflammatory diseases, hepatic macrophages are involved in their processing, and an increased level of these cells is detected in patients with fatty liver. Liver fibrosis is associated with physiological alterations in the anatomy and configuration of extracellular matrix of liver. Collagen type IV, proteoglycans, and laminin of subendothelial space are substituted by collagen type I and III leading to alteration in the hepatic architecture. It also exhibits a decreased production of matrix metalloproteinases as well as increased production of their inhibitors. Kupffer cells are known to participate in the above process and can be a target that can have significant role in management of this disease (Kolios et al., 2006).
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
High IL-18 serum levels are associated with psoriasis and AD (Gangemi et al. 2003; Sedimbi, Hägglöf, and Karlsson 2013; Tanaka et al. 2001). Psoriasis is correlated with an overexpression of Th1 cytokines and relative underexpression of Th2 cytokines. IL18 gene expression may play an important role in this disease by inducing Th1 response because IL-18 is a potent inductor of synthesis of IFN- γ, TNF-α and other mediators (Gangemi et al. 2003). Further, IL-18 may recruit DCs expressing IL-18 R to inflammatory areas under Th1 conditions as in psoriatic lesions (Lee, Cho, and Park 2015). When synergized with IL-23, IL-18 promotes development and maintenance of Th17 cells that were also implicated in developing the disease. Results from previous studies indicated that IL-18 serum or plasma levels correlate well with the Psoriasis Area and Severity Index (PASI) (Pietrzak et al. 2003; Takahashi et al. 2010). The expression of IL-18 was also elevated in initially active and progressive plaque-type psoriatic lesions (Companjen et al. 2004). Further, in cooperation with IL-23, IL-18 induced severe inflammation and enhanced psoriasis-like epidermal hyperplasia (Shimoura et al. 2017). Niu et al. (2019) using IL-18 knockout mouse model in imiquimod-induced psoriasis found that IL-18 promoted IL-17 mRNA expression and decreased IL-4 production, which may then prevent Th2 responses.
A new 1D Zn(II) coordination polymer containing pyridinyl-imidazolyl ligand: crystal structure and protective effect on dermatitis by reducing the inflammatory level
Published in Inorganic and Nano-Metal Chemistry, 2020
Geng Tian, Wei Liu, Zhi-Fang Zhang, Ji-Ping Liu
After treated with the dermatitis mice with nano 1 for 7 days. The IL-18, IL-33, TNF-α and total IgE levels in blood was measured by ELISA assay.[18] Briefly, the blood samples were harvested from the mice and centrifuged at 2,000 × g for 20 min at 4 °C for the serum samples collection. Serum IL-18 was measured by mouse IL-18 ELISA kit (MBL). Serum IL-33 was measured by mouse IL-33 e ELISA kit (R&D system). Serum TNF-α was measured by mouse TNF-α ELISA kit (R&D system). Total IgE was measured by mouse IgE ELISA kit (R&D system).