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Glycolytic and immunological alterations in human U937 monocytes in response to H1N1 infection
Author(s) -
Motawi Tarek Kamal,
Shahin Nancy Nabil,
Awad Kareem,
Maghraby Amany Sayed,
AbdElshafy Dideem,
Bahgat Mahmoud Mohamed
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2378
Subject(s) - tlr3 , tumor necrosis factor alpha , u937 cell , glycolysis , tlr7 , receptor , biology , monocyte , phosphofructokinase , immunology , chemistry , in vitro , toll like receptor , enzyme , biochemistry , innate immune system
We monitored changes that took place in glycolytic enzymes, the pyruvate end product of glycolysis, tumor necrosis factor α (TNFα), and toll‐like receptors (TLRs) both at the transcriptional and translational levels upon direct interaction between PR8‐H1N1 and the human monocytes U937 in vitro system. U937 were first treated with H1N1 infectious viral particles or phorbol‐12‐myristate‐13‐acetate (PMA) or left untreated and later infected with the H1N1 virus. Levels of phosphofructokinase 1 (PFK1) and pyruvate were biochemically quantified. In addition, levels of TNFα, TLR3, and TLR7 were measured by ELISA. The transcriptional profiles of PFKs, inflammatory cytokines, TLR3 and TLR7 were relatively quantified by qRT‐PCR. The results generally revealed significant changes in both the transcriptional and translational profiles of the studied biochemical and immunological parameters upon influenza infection in a time‐dependent manner. In conclusion, H1N1 infection triggers transcriptional and translational changes in immortalized human monocytes, which might serve as markers for infection subject for further validation for their specificities.