Beta-hemolysin-independent induction of apoptosis of macrophages infected with serotype III group B streptococcus

Abstract

Group B streptococcus (GBS) induces apoptosis in macrophages. Growth conditions minimizing beta-hemolysin expression, such as high glucose, reduce apoptosis. We constructed an isogenic mutant strain of GBS 874391 lacking the beta-hemolysin structural gene cylE and investigated the role that beta-hemolysin plays in apoptosis of J774 macrophages. Viability of macrophages infected with wild-type or cylE GBS was similar and significantly less than that of macrophages infected with GBS grown in high-glucose media. Thus, apoptosis in GBS-infected macrophages is dependent not on beta-hemolysin but on a factor coregulated with beta-hemolysin by glucose.