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. 2008 Dec 26;85(4):595–605. doi: 10.1189/jlb.1008631

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Fig. 5. — SR-A^+/−TLR4^+/− BMDC exhibit impaired kinetics of bacterial internalization and SR-A^+/−MyD88^+/− cells recapitulate this defect. (A) FACS histogram showing TLR4 cell-surface expression on BMDC from WT, TLR4^−/−, MyD88^+/−, and SR-A^+/−MyD88^+/− mice. MyD88 heterozygosity does not affect cell-surface expression of TLR4. (B) Gentamycin protection assays were performed on WT, MyD88^+/−, SR-A^+/−MyD88^+/−, and SR-A^−/− BMDC using E. coli bacteria. SR-A^+/−MyD88^+/− and SR-A^−/− BMDC showed significant impairment in phagocytosis of E. coli (*, P<0.05) compared with WT cells. For all graphs, n ≥ 18 for all genotypes, and the means and sd are shown. (C) Kinetic analysis of bacterial uptake was performed on WT, SR-A^+/−TLR4^+/−, SR-A^+/−MyD88^+/−, and SR-A^−/− BMDC. Quantitative uptake of bacteria by BMDC was assessed every 10 min using a gentamycin protection assay to determine the relative rates of phagocytosis for the indicated BMDC genotypes. SR-A^+/−TLR4^+/−, SR-A^+/−MyD88^+/−, and SR-A^−/− BMDC show impairment for the internalization of bacteria as early as 10 min after BMDC-bacteria coincubation, and this deficit is fully apparent by 20 min after bacterial exposure. For all graphs, the means and sd are shown.