Supplementary Tables S1 and S2

Skeletal muscles secrete a variety of cytokines in response to inflammatory stimuli such as lipopolysaccharides (LPS). However, the contributions of resident macrophages or other non-muscle cells to the cytokine secretory responses of muscle are not well understood. Here we tested the LPS-responsiveness of mouse soleus when a critical toll receptor adapter protein, (Myd88) was knocked out of all myeloid-derived cells (largely resident macrophages). The phenotype is referred to as LyzMyd88-/-. In solei from LyzMyd88-/- mice, cytokine secretory rates for IL-6 and KC(CXCL1) were reduced by ~50% during the first hour of LPS exposure compared to litter mate Myd88 controls. In the second hour of exposure, though G-CSF, IL-6, KC(CXCL1) and MCP-1(CCL2) were elevated nearly 5-10-fold compared to the first hour, only MCP-1 decreased secretion in LyzMyd88-/- muscles. We also tested the secretory response to buffer containing 1% sterile mouse plasma. Dilute plasma is known to amplify the responses of macrophages to LPS. One per cent plasma affected baseline measures of some cytokines but resulted in no further increases in cytokine secretion over either the first or second hour of exposure. However, both plasma-free and plasma-containing buffer induced small but significant increases in secretion of several cytokines over the sample collection period. Overall, the results are consistent with a significant early contribution of myeloid-derived, resident immune cells to the cytokine secretory responses in intact oxidative skeletal muscle.