FIG. 7.

SR-A^−/− BMMφ deficiency in bacterial phagocytosis is specific for SR-A. (A) BMMφ from SR-A^−/− or control ICR/129 mice were incubated with increasing doses of paraformaldehyde-fixed FITC-labelled E. coli DH5α or DiIAcLDL (inset) for 2 h and analyzed by flow cytometry. (B) SR-A^−/− or control 129/ICR Mφ were incubated with paraformaldehyde-fixed FITC-labelled E. coli DH5α (100 bacteria per Mφ) in the presence of an SR-A inhibitors, poly(I), or an inhibitor of phagocytosis, cytochalasin D (2 μM) (inset; the reduction in binding as well as ingestion may be because the major pool of SR-A is intracellular). To allow bacterial ingestion via the FcR, the FITC-labelled E. coli organisms were preincubated for 30 min with a rabbit anti-E. coli polyclonal antiserum in the absence of complement. The difference in mean fluorescence detected between 129/ICR and SR-A^−/− Mφ incubated with E. coli is significant (P < 0.001). The greater uptake by SR-A^−/− Mφ detected here was not reproducible and varied among experiments.