title: Attachment and invasion of Neisseria meningitidis to host cells is related to surface hydrophobicity, bacterial cell size and capsule.
abstract: We compared exemplar strains from two hypervirulent clonal complexes, strain NMB-CDC from ST-8/11 cc and strain MC58 from ST-32/269 cc, in host cell attachment and invasion. Strain NMB-CDC attached to and invaded host cells at a significantly greater frequency than strain MC58. Type IV pili retained the primary role for initial attachment to host cells for both isolates regardless of pilin class and glycosylation pattern. In strain MC58, the serogroup B capsule was the major inhibitory determinant affecting both bacterial attachment to and invasion of host cells. Removal of terminal sialylation of lipooligosaccharide (LOS) in the presence of capsule did not influence rates of attachment or invasion for strain MC58. However, removal of either serogroup B capsule or LOS sialylation in strain NMB-CDC increased bacterial attachment to host cells to the same extent. Although the level of inhibition of attachment by capsule was different between these strains, the regulation of the capsule synthesis locus by the two-component response regulator MisR, and the level of surface capsule determined by flow cytometry were not significantly different. However, the diplococci of strain NMB-CDC were shown to have a 1.89-fold greater surface area than strain MC58 by flow cytometry. It was proposed that the increase in surface area without changing the amount of anchored glycolipid capsule in the outer membrane would result in a sparser capsule and increase surface hydrophobicity. Strain NMB-CDC was shown to be more hydrophobic than strain MC58 using hydrophobicity interaction chromatography and microbial adhesion-to-solvents assays. In conclusion, improved levels of adherence of strain NMB-CDC to cell lines was associated with increased bacterial cell surface and surface hydrophobicity. This study shows that there is diversity in bacterial cell surface area and surface hydrophobicity within N. meningitidis which influence steps in meningococcal pathogenesis.
authors: School of Pathology and Laboratory Medicine, The University of Western Australia, Perth, Western Australia, Australia.
authors: Stephanie N
authors: SN
authors: Bartley
authors: Yih-Ling
authors: YL
authors: Tzeng
authors: Kathryn
authors: K
authors: Heel
authors: Chiang W
authors: CW
authors: Lee
authors: Shakeel
authors: S
authors: Mowlaboccus
authors: Torsten
authors: T
authors: Seemann
authors: Wei
authors: W
authors: Lu
authors: Ya-Hsun
authors: YH
authors: Lin
authors: Catherine S
authors: CS
authors: Ryan
authors: Christopher
authors: C
authors: Peacock
authors: David S
authors: DS
authors: Stephens
authors: John K
authors: JK
authors: Davies
authors: Charlene M
authors: CM
authors: Kahler
mesh_terms: D001422:Bacterial Adhesion / Q000502:physiology*; D015153:Blotting, Western; D001980:Bronchi / Q000378:metabolism*; D048429:Cell Size; D002478:Cells, Cultured; D024202:Electrophoretic Mobility Shift Assay; D010861:Fimbriae, Bacterial / Q000378:metabolism; D005434:Flow Cytometry; D006031:Glycosylation; D006801:Humans; D057927:Hydrophobic and Hydrophilic Interactions; D008070:Lipopolysaccharides / Q000378:metabolism*; D008589:Meningococcal Infections / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D019158:N-Acetylneuraminic Acid / Q000378:metabolism; D009345:Neisseria meningitidis / Q000378:metabolism* / Q000472:pathogenicity*; D010610:Pharyngeal Neoplasms / Q000378:metabolism / Q000382:microbiology* / Q000473:pathology; D010641:Phenotype; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D008070:Lipopolysaccharides; D012333:RNA, Messenger; C023023:lipid-linked oligosaccharides; D019158:N-Acetylneuraminic Acid