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10.1097/SHK.0000000000000169

http://scihub22266oqcxt.onion/10.1097/SHK.0000000000000169
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C4071940!4071940!24667630
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suck abstract from ncbi


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pmid24667630      Shock 2014 ; 42 (1): 52-9
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  • Itraconazole, A Commonly Used Antifungal, Inhibits Fc? Receptor-Mediated Phagocytosis: Alteration of Fc? Receptor Glycosylation And Gene Expression* #MMPMID24667630
  • Niņo DF; Cauvi DM; De Maio A
  • Shock 2014[Jul]; 42 (1): 52-9 PMID24667630show ga
  • Itraconazole (ICZ)? is commonly used for the treatment of fungal infections, particularly in immunocompromised patients. In addition, ICZ has been recently found to have anti-angiogenic effects and is currently being tested as a new chemotherapeutic agent in several cancer clinical trials. We have previously shown that ICZ impaired complex N-linked glycosylation processing, leading to the accumulation of high-mannose glycoproteins on the surface of macrophages. This investigation was directed at determining the effects of ICZ on phagocytosis as a major function of macrophages. We found a significant decrease in the phagocytosis of opsonized bacterial particles in ICZ-treated murine macrophages in comparison with non-treated macrophages. Furthermore, the impairment of phagocytosis was associated with a decrease in cell surface expression of Fc? receptors (Fc?R) as well as alteration of their glycosylation pattern. Concomitantly, a reduction in all three isoforms of the Fc?R family (i.e., Fcgr1, Fcgr2 and Fcgr3) mRNA levels was observed after incubation with ICZ. The effect of ICZ on phagocytosis and Fc?R expression was reversed by addition of LDL. These studies indicate that ICZ treatment certainly has a dramatic effect on macrophage function, which could result in a potential impairment of the immune system's ability to respond to pathogens and may lead to elevated incidence of infections.
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