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.

Disease and Carrier Isolates of Neisseria meningitidis Cause G 1 Cell Cycle Arrest in Human Epithelial Cells

“…Detroit 562 cells are commonly used for N. meningitidis host cell interaction studies and exhibit high levels of bacterial adhesion (51)(52)(53). This cell line has been shown to express high levels of carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), a major Opa receptor, after exposure to cytokines or when infected with Opa-expressing N. meningitidis (52).…”

“…Moreover, the meningococcal wild-type strain MC58 elicited a time-dependent increase of uptake. In addition, the isogenic unencapsulated mutant showed a significantly higher rate of invasion compared to the wild-type strain due to the inhibitory effect of the serogroup B capsule polysaccharide of strain MC58 to bacterial invasion (22,23,32,51,56). We observed that meningococcal disease strain 8013/clone12 and carrier isolate ␣711 effectively adhered to Detroit 562 cells, whereas they were poorly invasive for both epithelial cell lines.…”

Expression of factor H binding protein in meningococcal strains can vary at least 15-fold and is genetically determined

“…We found that in the case of the MC58 strain the surface area is 4.98 μm . Considering MC58 as the reference strain, and assuming that only marginal differences exist in the dimensions of meningococcal strains (20), the distance between adjacent molecules on isolates expressing fHbp at levels compatible with SBA data (Table 1) ranges between 33 nm (strain M08-0240104, n = 9,390) and 115 nm (calculated average distance between two fHbp molecules) ( Table 2 and Fig. 4), whereas bacteria with negative SBA had a distance between molecules of 130 nm or more.…”

Neisseria meningitidis Polynucleotide Phosphorylase Affects Aggregation, Adhesion, and Virulence

“…5A). Because the capsule is much more hydrophilic than the underlying bacterial cell surface, the degree of capsulation can also be determined by measuring cellular hydrophobicity (54). We measured hydrophobicity using MATS (microbial adhesion to solvents) assays (47).…”