NafA negatively controls Neisseria meningitidis piliation
2011 (English)In: PLoS ONE, ISSN 1932-6203, Vol. 6, no 7, e21749- p.Article in journal (Refereed) Published
Bacterial auto-aggregation is a critical step during adhesion of N. meningitidis to host cells. The precise mechanisms and functions of bacterial auto-aggregation still remain to be fully elucidated. In this work, we characterize the role of a meningococcal hypothetical protein, NMB0995/NMC0982, and show that this protein, here denoted NafA, acts as an anti-aggregation factor. NafA was confirmed to be surface exposed and was found to be induced at a late stage of bacterial adherence to epithelial cells. A NafA deficient mutant was hyperpiliated and formed bundles of pili. Further, the mutant displayed increased adherence to epithelial cells when compared to the wild-type strain. In the absence of host cells, the NafA deficient mutant was more aggregative than the wild-type strain. The in vivo role of NafA in sepsis was studied in a murine model of meningococcal disease. Challenge with the NafA deficient mutant resulted in lower bacteremia levels and mortality when compared to the wild-type strain. The present study reveals that meningococcal NafA is an anti-aggregation factor with strong impact on the disease outcome. These data also suggest that appropriate bacterial auto-aggregation is controlled by both aggregation and anti-aggregation factors during Neisseria infection in vivo.
Place, publisher, year, edition, pages
2011. Vol. 6, no 7, e21749- p.
IdentifiersURN: urn:nbn:se:su:diva-63671DOI: 10.1371/journal.pone.0021749ISI: 000292293400029PubMedID: 21747953OAI: oai:DiVA.org:su-63671DiVA: diva2:451666