Only those mice with blood glucose levels greater than 20 mmol/l were used as recipients

cell line (Maf-DKO cells). In these cells, oligomycin treatment had no effect at all, while 2-DG inhibited Maf-DKO phagocytosis to the same extend as in RAW 264.7 cells (Figure S2A, B). Upon total glucose deprivation (by substitution with galactose), the phagocytic index in both RAW 264.7 and Maf-DKO cells dropped immediately below 20% (Figure 6E and Figure S2C). An even bigger drop was seen in RAW 264.7 cells after 4 and 14 hours (Figure 6E). It is important to note that at 0 and 4 hours the cells were still fully viable. Thus, we conclude that the reduction in phagocytic activity must be solely the result of insufficiency in glucose availability and not be a secondary effect of functional incapacitation. The low phagocytic index in the absence of glucose was accompanied by a reduction in particle internalization efficiency (Figure 6F) as well as a reduction in the binding capacity of the cells since the percentage of FITC-COZ positive cells was also reduced by more than 50% (results not shown). These results suggest that glucose availability is essential for both particle binding and internalization. Interestingly, and in keeping with this conclusion, supplementation of galactose medium with 1 mM glucose enabled the cells to maintain full phagocytosis capacity (Figure 6G&H). May 2014 | Volume 9 | Issue 5 | e96786 Glucose Controls Macrophage Morphodynamics Figure 3. Actin cytoskeletal structural changes induced by inhibition of glycolysis or mitochondrial OXPHOS. RAW 264.7 cells were seeded on glass coverslips, incubated in control medium or medium containing 2.5 mM oligomycin and 25 mM glucose (A�F), 10 mM 2-DG and 25 mM glucose (G�J), 10 mM galactose and no AZD-0530 cost PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19652729 glucose (M�P), or 1 mM glucose and 10 mM galactose (Q�T) for th