Streptococcus pneumoniae–Associated Human Macrophage Apoptosis after Bacterial Internalization via Complement and Fcγ Receptors Correlates with Intracellular …

F Ali, ME Lee, F Iannelli, G Pozzi… - The Journal of …, 2003 - academic.oup.com
F Ali, ME Lee, F Iannelli, G Pozzi, TJ Mitchell, RC Read, DH Dockrell
The Journal of infectious diseases, 2003academic.oup.com
Opsonization enhances Streptococcus pneumoniae–induced human monocyte–derived
macrophage (MDM) apoptosis. Both depletion of complement and immunoglobulin from
opsonizing serum and blockade of the macrophages CR1, CR3, FcγRII, and FcγRIII partially
decreased MDM apoptosis after S. pneumoniae phagocytosis, and these effects correlated
with reduced numbers of internalized bacteria. Chloramphenicol inhibition of protein
synthesis by opsonized S. pneumoniae down-regulated subsequent MDM apoptosis …
Abstract
Opsonization enhances Streptococcus pneumoniae–induced human monocyte–derived macrophage (MDM) apoptosis. Both depletion of complement and immunoglobulin from opsonizing serum and blockade of the macrophages CR1, CR3, FcγRII, and FcγRIII partially decreased MDM apoptosis after S. pneumoniae phagocytosis, and these effects correlated with reduced numbers of internalized bacteria. Chloramphenicol inhibition of protein synthesis by opsonized S. pneumoniae down-regulated subsequent MDM apoptosis. Phagocytosis of an unencapsulated mutant of S. pneumoniae resulted in increased MDM apoptosis, in association with enhanced internalization. Caspase inhibition was associated with decreased killing of bacteria. Enhanced induction of apoptosis by opsonized S. pneumoniae is the result of increased intracellular burden of bacteria, rather than of a specific pattern of engagement of complement receptor or FcγR. A dynamic interaction between live intracellular bacteria and the host cell is necessary for induction of apoptosis in MDMs, and induction of apoptosis contributes to the host defense against S. pneumoniae
Oxford University Press