Reporting in the open-access journal PLoS Biology, Magdalene So and colleagues present evidence that bacteria can induce changes in hosts' gene expression - and possibly keep the host cells alive longer - through tiny tugs on cell membranes. The study examined gene activity in human epithelial cells infected with Neisseria gonorrhoeae, the bacteria responsible for the sexually transmitted disease gonorrhea.
By comparing cells infected with normal N. gonorrhoeae to those infected with a mutant strain with defective pili, the researchers found a subset of 52 host genes that had higher activity when the host was infected with the normal bacteria, suggesting that the pulls of the pili were responsible. They then showed that an artificial mechanical pull on the host cell membrane could trigger a signaling cascade in the host cells to affect the host's gene expression.
Many of the genes that increased in activity due to the tugs were already known to regulate apoptosis and cellular response to stress, including mechanical strain on the membrane. Also, a majority of these genes were known to be induced by a family of proteins called mitogen-activated protein kinases, or MAPKs. The researchers showed that blocking MAPKs reduced the activity of several of the genes that are usually enhanced by infection with the normal bacteria. Also, they found that cells infected with the bacteria tended to survive treatment with staurosporine, a chemical that normally induces apoptosis.
Overall, the group's findings support previous speculations that some bacteria influence gene expression and the fate of cells in their hosts by tugging on the host cells' membranes with their pili. For bacteria like N. gonorrhoeae that pass directly from host to host, the researchers argue, it would be in a bacterium's interest to help keep its host alive. And bacteria appear to do this with the help of their pili.
Citation: Howie HL, Glogauer M, So M (2005) The Neisseria gonorrhoeae type IV pilus stimulates mechanosensitive pathways and cytoprotection through a pilT-dependent mechanism. PLoS Biol 3(4): e100.
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