title: Association and virulence gene expression vary among serotype III group B streptococcus isolates following exposure to decidual and lung epithelial cells.
abstract: Group B Streptococcus (GBS) causes severe disease in neonates, the elderly, and immunocompromised individuals. GBS species are highly diverse and can be classified by serotype and multilocus sequence typing. Sequence type 17 (ST-17) strains cause invasive neonatal disease more frequently than strains of other STs. Attachment and invasion of host cells are key steps in GBS pathogenesis. We investigated whether four serotype III strains representing ST-17 (two strains), ST-19, and ST-23 differ in their abilities to attach to and invade both decidual cells and lung epithelial cells. Virulence gene expression following host cell association and exposure to amnion cells was also tested. The ST-17 strains differed in their abilities to attach to and invade decidual cells, whereas there were no differences with lung epithelial cells. The ST-19 and ST-23 strains, however, attached to and invaded decidual cells less than both ST-17 strains. Although the ST-23 strain attached to lung epithelial cells better than ST-17 and -19 strains, none of the strains effectively invaded the lung epithelial cells. Notably, the association with host cells resulted in the differential expression of several virulence genes relative to basal expression levels. Similar expression patterns of some genes were observed regardless of cell type used. Collectively, these results show that GBS strains differ in their abilities to attach to distinct host cell types and express key virulence genes that are relevant to the disease process. Enhancing our understanding of pathogenic mechanisms could aid in the identification of novel therapeutic targets or vaccine candidates that could potentially decrease morbidity and mortality associated with neonatal infections.
authors.affiliation: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
authors.forename: Michelle L
authors.initials: ML
authors.lastname: Korir
authors.affiliation: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
authors.forename: David
authors.initials: D
authors.lastname: Knupp
authors.affiliation: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
authors.forename: Kathryn
authors.initials: K
authors.lastname: LeMerise
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Erica
authors.initials: E
authors.lastname: Boldenow
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, Michigan, USA.
authors.forename: Rita
authors.initials: R
authors.lastname: Loch-Caruso
authors.affiliation: Division of Infectious Diseases, Department of Medicine, Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
authors.forename: David M
authors.initials: DM
authors.lastname: Aronoff
authors.affiliation: Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA mannin71@msu.edu.
authors.forename: Shannon D
authors.initials: SD
authors.lastname: Manning
mesh_terms: D002460:Cell Line; D003656:Decidua / Q000166:cytology*; D004847:Epithelial Cells / Q000502:physiology*; D005260:Female; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D006801:Humans; D008168:Lung / Q000166:cytology*; D013292:Streptococcus agalactiae / Q000145:classification / Q000235:genetics / Q000378:metabolism* / Q000472:pathogenicity*; D014774:Virulence