August 25, 2010
Bacterial Pathogens Delay Their Entry Into Cells
Pathogens make themselves feel at home in the human body, invading cells and living off the plentiful amenities on offer. However, researchers at the Max Planck Institute for Infection Biology, Berlin, together with colleagues at Harvard University, reveal an opposite strategy used to ensure infection success. Pathogens can actually delay their entry into cells to ensure their survival. Upon cell contact, bacteria trigger a local strengthening of the cellular skeleton with the aid of signaling molecules, allowing them to remain outside the cell. The researchers also show that this strategy, unknown until now, is used by certain intestinal pathogens as well. (PLoS Biology, August 24, 2010)
Infection with the sexually transmitted bacterium Neisseria gonorrhoeae can lead to an inflammation of the urogenital tract, the uterus and ovaries. By means of thread-shaped proteins on its surface called pili, the bacterium attaches itself to the cell membrane. Once attached, the bacteria undergo rapid changes of their surface structure to avoid recognition by the host's immune system. Only during the later stages of infection will the pathogens penetrate cells and occasionally advance into deeper tissues to find further breeding ground.
Better outside than inside
These results have opened up new perspectives in understanding the course of infections: "For a long time it was thought that most pathogens strive to enter cells quickly. However, the opposite may be the case. It seems the bacteria prolong their extracellular existence in order to survive", declares Thomas F. Meyer of the Max Planck Institute of Infection Biology. By anchoring to the cell via pili proteins and assembling an underlying support skeleton, the pathogen is buffered against the often inhospitable conditions of the extracellular environment.
By extrapolating their findings to the intestinal bacteria Escherichia coli, the scientists have indicated that the strategy of delaying entry into cells to ensure survival may be widespread among pathogens, possibly even the bacterial agents of meningitis and pneumonia. These newly discovered signaling pathways may therefore have exciting implications for the prevention of infection.
Original work: Jan Peter Boettcher, Marieluise Kirchner, Yuri Churin, Alexis Kaushansky, Malvika Pompaiah, Hans Thorn, Volker Brinkmann, Gavin MacBeath, Thomas F. Meyer. Tyrosine-phosphorylated caveolin-1 blocks bacterial uptake by inducing Vav2-RhoA-mediated cytoskeletal rearrangements. PLoS Biology, August 24, 2010
Image Caption: Neisseria gonorrhoeae bacteria, forming micro-colonies on the surface of a human cell, stimulate signals to stabilize their extracellular life style. Image: Max Planck Institute for Infection Biology
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