Abstract
Streptococcus agalactiae (group B streptococcus or GBS) is a commensal bacterium that can frequently behave as a pathogen, particularly in the neonatal period and in the elderly. The gut is a primary site of GBS colonization and a potential port of entry during neonatal infections caused by hypervirulent clonal complex 17 (CC17) strains. Here we studied the interactions between the prototypical CC17 BM110 strain and polarized enterocytes using the Caco-2 cell line. GBS could adhere to and invade these cells through their apical or basolateral surfaces. Basolateral invasion was considerably more efficient than apical invasion and predominated under conditions resulting in weakening of cell-to-cell junctions. Bacterial internalization occurred by a mechanism involving caveolae- and lipid raft-dependent endocytosis and actin re-organization, but not clathrin-dependent endocytosis. In the first steps of Caco-2 invasion, GBS colocalized with the early endocytic marker EEA-1, to later reside in acidic vacuoles. Taken together, these data suggest that CC17 GBS selectively adheres to the lateral surface of enterocytes from which it enters through caveolar lipid rafts using a classical, actin-dependent endocytic pathway. These data may be useful to develop alternative preventive strategies aimed at blocking GBS invasion of the intestinal barrier.
Highlights
Streptococcus agalactiae or group B streptococcus (GBS) is a Gram-positive bacterium that can cause invasive disease, including sepsis and meningitis [1]
GBS were found in the intercellular spaces of large 5-day-old islands, in optical sections corresponding to the parabasal levels of the vertical cell axis (S2 Fig)
In 21-day-old monolayers, only small numbers of bacteria were visible, and these colocalized to apical, but not subapical, sections (Fig 1C). These results indicate that hypervirulent GBS adheres preferentially to the lateral surfaces of Caco-2 cells at subapical and parabasal sites along the vertical cell axis
Summary
Streptococcus agalactiae or group B streptococcus (GBS) is a Gram-positive bacterium that can cause invasive disease, including sepsis and meningitis [1]. Neonatal GBS disease occurring during the first week of life is defined as early-onset disease (EOD) and is often initiated by aspiration of secretions from the genital tract of colonized mothers during parturition [2]. Disease occurring from day 8 to 89 after birth is defined as late onset disease (LOD) [2, 3]. Meningitis is frequent in LOD and can be followed by permanent neurological disorders [4]. GBS frequently colonizes the gut and the genital tract and its ability to adhere to mucosal epithelial cells is an essential factor in these activities [2, 3]. Invasion of epithelial barriers is an obligatory event in pathogenesis [7, 8]
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