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Hyperthermia potentiates the IL‐6 mRNA response to LPS in C2C12 muscle cells
Author(s) -
Welc Steven S,
Chen Dan L.,
Clanton Thomas L.
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1083.4
Subject(s) - myogenesis , messenger rna , c2c12 , hyperthermia , skeletal muscle , immune system , chemistry , myocyte , heat shock protein , innate immune system , microbiology and biotechnology , endocrinology , medicine , biology , immunology , biochemistry , gene
In heat stroke and bacterial infection, skeletal muscles (SM) can be exposed simultaneously to hyperthermia (HT) and endotoxin. Both are potent stimuli of IL‐6 in SM. We hypothesized that when these stimuli act together they potentiate SM IL‐6 production, which could implicate a role for SM in whole body innate immune responses. Aims 1) to treat C2C12 cells with LPS or LPS+HT (42°C) and compare IL‐6 mRNA at 1, 2, 3, and 6 h, 2) to compare IL‐6 protein between treatments, and 3) to compare the response of myoblasts (MYOB) and myotubes (MYOT) to these co‐stimuli. Cells were supplemented with LPS (1 ug/ml) and simultaneously exposed to 37°C or 42°C for 1 h, then harvested or allowed to recover at 37°C for 1, 2, or 5 h. In a separate experiment, MYOT were treated with LPS (1000, 100, 10, and 1 ng/ml) and the supernatant was sampled at 6 h and analyzed for IL‐6 protein. Significant up regulation of IL‐6 mRNA was seen in MYOB and MYOT in response to LPS (P<0.05). Furthermore, the addition of HT potentiated the increase of IL‐6 mRNA compared to LPS alone (P<0.05); the amplification spanned 3h (MYOB) and 6 h (MYOT). Interestingly, IL‐6 protein was either not different or attenuated in HT+LPS vs. LPS. Results further demonstrate that HT is a functional stimulus for IL‐6 mRNA, possibly part of the HSF‐initiated heat shock response. We speculate variations in IL‐6 protein are a consequence of translational inhibition associated with mild heat shock. Supported by: AHA #11GRNT7990119