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Tug-of-War: How bacteria prevent host-cell suicide

Christen Brownlee

When they battle bacteria, animal cells have a surefire way to keep infection from spreading: They drop dead. New research suggests that with tiny tugs on the attacked cells' membranes, bacteria may pester the cells into living longer—and keeping infections going strong.

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HAIRY SITUATION. This Neisseria gonorrhoeae bacterium may keep its host's cells alive with tugs from its pili, seen as dark strands around the cell.

S. Lee

When an infected host's cells die, they eliminate resources that the bacteria use to stay alive and spread. This self-sacrifice may save the animal's life. But when too many host cells die, bacteria can kill a host before they're ready to jump ship—thus hurting the bacterial species' chances for survival.

To get some insight into why host cells live long enough to support bacterial infections, Magdalene So of Oregon Health and Science University in Portland and her colleagues worked with Neisseria gonorrhoeae, the bacterial species that causes gonorrhea in people.

N. gonorrhoeae has pili, which are hairlike structures that bacteria extend and retract to move and to retrieve needed items.

After infecting lab-grown human cells with normal N. gonorrhoeae and a mutant strain that doesn't make pili, So's team examined host-gene expression. Infection by either strain turned on the same 300 or so human genes. However, the researchers found that a subset of 52 genes was more active in cells infected with the normal bacteria.

About half the genes in this group produce proteins that signal cells to stay alive through stressful situations, says So.

The thousands of bacteria in a colony can use their pili to tug on host cells with considerable total force—about 10,000 piconewtons, which So says is about the force of a human bite. She and her colleagues hypothesized that tugs from pili cause cells to stay alive during an infection.

To investigate whether mechanical force could produce similar results in uninfected cells, So's team attached tiny metal beads to the surface of human cells. After tugging on the cells with a magnet, the researchers found increased activity in the set of 52 genes.

"We were able to replicate [gene expression in] infection just by pulling on the cell," says So. Her team will publish these findings in the April PLoS Biology.

Dale Kaiser, a microbiologist at Stanford University School of Medicine, calls the findings interesting. He says, however, that he's skeptical that evolution led the bacterium to tug on cell membranes in just the right way to lengthen the cells' survival.

Kaiser notes that many bacterial species use pili to suck food from host cells. "I think that from the point of view of the bacterium, it's just trying to eat," he says.

Staying alive to host the bacterium might just be a side effect of the stress response that helps cells survive other adverse circumstances, comments So. "When you're faced with a life-or-death situation, you're better able to deal with it if you're all hopped up," she says.

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References:

Howie, H.L., M. Glogauer, and M. So. 2005. The N. gonorrhoeae type IV pilus stimulates mechanosensitive pathways and cytoprotection through a pilT-dependent mechanism. PLoS Biology 3(April):e100. Full Text.

Further Readings:

Binnicker, M.J., R.D. Williams, and M.A. Apicella. 2003. Infection of human urethral epithelium with Neisseria gonorrhoeae elicits an upregulation of host anti-apoptotic factors and protects cells from staurosporine-induced apoptosis. Cellular Microbiology 5(August):549–560. Abstract.

Wall, D., and D. Kaiser. 1999. Type IV pili and cell motility. Molecular Microbiology 32(April):1–10. Abstract.

Sources:

Dale Kaiser
Stanford University School of Medicine
Department of Biochemistry
Beckman Center B400
279 W. Campus Drive, MC: 5307
Stanford, CA 94305

Magdalene So
Oregon Health and Science University
Department of Molecular Microbiology and Immunology
3181 S.W. Sam Jackson Park Road
Portland, OR 97239-3098


From Science News, Volume 167, No. 13, March 26, 2005, p. 196.