title: Ability of clinical isolates of group A streptococci to adhere to and invade HEp-2 epithelial cells.
abstract: Individual strains of group A streptococci (GAS) differ in virulence, but the reasons for these differences are incompletely understood. To determine if the ability of GAS to cause invasive disease corresponded with their capacity to adhere to or invade epithelial cells, 63 clinical isolates of GAS (40 from patients with systemic infection and 23 from superficial disease) were examined in quantitative assays of bacterial adhesion to and invasion of HEp-2 cells, a continuous line of human pharyngeal epithelial cells. The results showed that individual isolates of GAS varied considerably in their ability to adhere to and penetrate HEp-2 cells. However, on the whole, strains from patients with invasive disease adhered to cells in numbers c.1.5 greater than those from superficial infection. Paradoxically, strains from patients with invasive disease invaded HEp-2 cells to a significantly lesser extent than those from superficial sites, with a two-fold difference in invasion index (defined as the percentage of cell-associated bacteria located intracellularly). To determine if these differences were caused by differences in the production of hyaluronic acid capsule or M protein by the two groups of bacteria, the adherence and invasive capacities of bacteria carrying defined mutations in the genes for these factors were examined. Although M6-protein-deficient [corrected] bacteria were less adherent to HEp-2 cells than the wild-type, neither the hyaluronic acid capsule nor the M protein had a significant influence on the ability of GAS to adhere to or invade HEp-2 cells. The results of this study demonstrate that there are biological differences between GAS isolates associated with invasive and superficial diseases and that these differences can be demonstrated by an assay of bacterial adherence to and invasion of HEp-2 epithelial cells.
authors.affiliation: Department of Microbiology and Infectious Diseases, Royal Children's Hospital, University of Melbourne, Parkville, Victoria, Australia.
authors.forename: V R
authors.initials: VR
authors.lastname: Bennett-Wood
authors.forename: J R
authors.initials: JR
authors.lastname: Carapetis
authors.forename: R M
authors.initials: RM
authors.lastname: Robins-Browne
mesh_terms: D000328:Adult; D000942:Antigens, Bacterial; D001422:Bacterial Adhesion; D016667:Bacterial Capsules / Q000737:chemistry / Q000502:physiology; D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins / Q000032:analysis / Q000502:physiology; D002352:Carrier Proteins; D002648:Child; D004847:Epithelial Cells / Q000382:microbiology*; D006801:Humans; D006820:Hyaluronic Acid / Q000032:analysis; D008854:Microscopy, Electron; D010610:Pharyngeal Neoplasms; D010614:Pharynx / Q000166:cytology / Q000382:microbiology*; D013290:Streptococcal Infections / Q000382:microbiology* / Q000473:pathology; D013297:Streptococcus pyogenes / Q000145:classification / Q000472:pathogenicity* / Q000648:ultrastructure; D014407:Tumor Cells, Cultured; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D001426:Bacterial Proteins; D002352:Carrier Proteins; C014689:streptococcal M protein; D006820:Hyaluronic Acid