Although, neutrophils are capable to engulf and kill most microorganisms, Neisseria is remarkably resistant to neutrophil killing. Severe meningococcal disease is characterized by early neutrophil activation and an accumulation of neutrophils into the subarachnoidal space is one of the hallmarks of N. meningitidis infection. Several mechanisms have been described that explain how Neisseria cross the epithelium: through damaged epithelial layers; the transcellular route; depletion of junctional proteins followed by an opening at the cell-cell interface; and via a “Trojan horse” manner inside phagocytes.

Helena Aro’s research group are studying type IV pilus-mediated adherence of pathogenic Neisseria to the uropod (the rear) of polarized PMNs. 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.

 

 
SEM electrograph showing the specificity of bacterial adherence to the uropod of a polarized PMN.
SEM electrograph showing the specificity of bacterial adherence to the uropod of a polarized PMN. Photo: Niklas Söderholm
 

 

 

Polymorphonuclear neutrophils (PMNs) are important components of the human innate immune system and are rapidly recruited at the site of bacterial infection. We have revealed a novel type IV pilus-mediated adherence of pathogenic Neisseria to the uropod (the rear) of polarized PMNs. This movie shows new mechanism where pathogenic Neisseria can hitchhike on the uropod of PMNs and thereby avoid their phagocytic activity and simultaneously increase their ability to spread over the epithelial cell layer.

 

Live-cell imaging of PMNs suggested that bacterial adherence to the uropod is followed by internalization into PMNs via the uropod. The movie shows DyLight NHS ester-stained bacteria (green) invades freshly isolated human PMNs that were stained with fluorescent labeled Lysotracker (red).