نبذة مختصرة : Sialic acids (SAs) are the terminal sugars of cell surface glycoconjugates and are the critical determinants in many physiological and pathological processes. Macrophage cell surface expresses a dense layer of glycans often terminated with SAs which are involved in many biological processes of macrophages such as host‐pathogen recognition, migration, and antigen presentation. Notably, humans make Neu5Ac but are incapable of synthesizing Neu5Gc. However, humans can incorporate Neu5Gc into glycoconjugates through dietary acquisition. Neu5Gc‐containing glycoconjugates can be immunogenic and associated with many diseases and disease progressions such as cancer and cancer development. Moreover, the Neu5Gc‐containing glycoconjugates contribute to infectious diseases as they can serve as receptors for pathogens or toxin. Because the incorporation of Neu5Gc carries negative consequences for humans, we investigated if human macrophage cells may intake Neu5Gc under different condition and have some effects on its functions. Here, we utilized THP‐1 macrophages as a model to examine its Neu5Ac and Neu5Gc intake under the normal and inflammatory condition which was induced by lipopolysaccharide (LPS). LC‐MS/MS was used to quantify the total Neu5Ac and Neu5Gc changes, and cell surface SAs lectin bindings confirmed by flow cytometry analysis. Also, their phagocytosis capacity was evaluated upon Neu5Ac and Neu5Gc under inflammatory conditions. Overall, we found that THP‐1 macrophages has a different intake of Neu5Ac and Neu5Gc under different conditions and affect its phagocytosis as well. Support or Funding Information This work was supported by Faculty Research Development Fund and the research fund from the Center for Gene Regulation in Health and Disease (GRHD) at Cleveland State University supported by Ohio Department of Development (ODOD). The authors acknowledge the National Science Foundation Major Research Instrumentation Grants for supporting NMR and QTrap 5500 mass spectrometer instrument requisition at Cleveland ...
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