Abstract
Polymorphonuclear neutrophils (PMNs) are important components of the human innate immune system and are rapidly recruited at the site of bacterial infection. Despite the effective phagocytic activity of PMNs, Neisseria gonorrhoeae infections are characterized by high survival within PMNs. We reveal a novel type IV pilus-mediated adherence of pathogenic Neisseria to the uropod (the rear) of polarized PMNs. The direct pilus-uropod interaction was visualized by scanning electron microscopy and total internal reflection fluorescence (TIRF) microscopy. We showed that N. meningitidis adhesion to the PMN uropod depended on both pilus-associated proteins PilC1 and PilC2, while N. gonorrhoeae adhesion did not. Bacterial adhesion elicited accumulation of the complement regulator CD46, but not I-domain-containing integrins, beneath the adherent bacterial microcolony. Electrographs and live-cell imaging of PMNs suggested that bacterial adherence to the uropod is followed by internalization into PMNs via the uropod. We also present data showing that pathogenic Neisseria can hitchhike on PMNs to hide from their phagocytic activity as well as to facilitate the spread of the pathogen through the epithelial cell layer.
Highlights
The genus Neisseria includes the two obligate human pathogens N. gonorrhoeae and N. meningitidis
Using live cell imaging techniques, we demonstrate a new mechanism where pathogenic Neisseria can hitchhike on the uropod of Polymorphonuclear neutrophils (PMNs) and thereby avoid the phagocytic activity of the PMNs and simultaneously increase their ability to spread at the epithelial cell layer
The uropod was distinguished from the pseudopod by the fact that the uropod is at the rear of the migrating PMN
Summary
The genus Neisseria includes the two obligate human pathogens N. gonorrhoeae and N. meningitidis. Bacteria can enter the meninges from the nasopharynx by redistribution of the intracellular junction protein N-cadherin in olfactory epithelia [3]. These two species of bacteria cause different diseases, the molecular mechanisms during infection are similar and they share many important virulence factors involved in both adhesion to and invasion of epithelial cells. In N. gonorrhoeae, both PilC1 (pilC2D)- and PilC2 (pilC1D)-expressing bacteria adhere to epithelial cells, while only PilC1 (pilC2D)-expressing N. meningitidis mediate adherence [21,22,23]. Morand et al reported that meningococcal PilC2 mediated adhesion to epithelial cells [19]
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