Abstract
Infections by Neisseria meningitidis show duality between frequent asymptomatic carriage and occasional life-threatening disease. Bacterial and host factors involved in this balance are not fully understood. Cytopathic effects and cell damage may prelude to pathogenesis of isolates belonging to hyper-invasive lineages. We aimed to analyze cell–bacteria interactions using both pathogenic and carriage meningococcal isolates. Several pathogenic isolates of the ST-11 clonal complex and carriage isolates were used to infect human epithelial cells. Cytopathic effect was determined and apoptosis was scored using several methods (FITC-Annexin V staining followed by FACS analysis, caspase assays and DNA fragmentation). Only pathogenic isolates were able to induce apoptosis in human epithelial cells, mainly by lipooligosaccharide (endotoxin). Bioactive TNF-α is only detected when cells were infected by pathogenic isolates. At the opposite, carriage isolates seem to provoke shedding of the TNF-α receptor I (TNF-RI) from the surface that protect cells from apoptosis by chelating TNF-α. Ability to induce apoptosis and inflammation may represent major traits in the pathogenesis of N. meningitidis. However, our data strongly suggest that carriage isolates of meningococci reduce inflammatory response and apoptosis induction, resulting in the protection of their ecological niche at the human nasopharynx.
Highlights
Neisseria meningitidis is the causative agent of meningococcal meningitis and fulminant sepsis
Acquisition of Neisseria meningitidis often leads to asymptomatic colonization and rarely results in invasive disease associated with tissue injury
We aimed to investigate the cytopathic effect of meningococcal isolates on epithelial cells using both Sequence types (ST)-11 pathogenic isolates and carriage isolates
Summary
Neisseria meningitidis is the causative agent of meningococcal meningitis and fulminant sepsis. There is increasing evidence that invasive meningococcal infections lead to cytopathic effects that often result in marked tissue and cell damage mainly characterized by the breakdown of cell tight junctions, the deterioration of the cell layers, changes in normal cell morphology, and loss of cells [2,3,4,5,6,7,8]. These observations are consistent with the extensive tissue damage and cell death seen in autopsy material from fatal human cases [9]. Various components of the bacterial cell wall are capable of activating proinflammatory response, notably the meningococcal lipooligosaccharide (LOS), the major structural component of the outer membrane
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