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Chlamydia parasite lives off our fat

not amenable to direct genetic manipulation so the researchers moved the pathogen's genes elsewhere, inserting them into the eukaryotic cells of baker's yeast. The resulting chlamydial proteins were screened for those that targeted to yeast intracellular organelles. They identified four proteins that were specifically recruited to lipid droplets.

The researchers found that Chlamydia not only directs lipid droplets to its protective vacuole but also causes the proliferation of new lipid droplets on the host. The co-option of lipid droplets appears to be essential for Chlamydia pathogenesis. When the researchers used drugs to inhibit lipid droplet formation in the host, they sharply impaired bacterial growth.

That finding immediately presents a new target for anti-Chlamydia drugs but it also suggests an entirely novel pathogenic mechanism. "We propose that Chlamydia use lipid droplets in a previously unknown pathway for lipid acquisition," says Kumar. "Alternatively, it is possible that the recruitment of lipid droplets constitutes an example of 'organelle mimicry' where Chlamydia escapes recognition by the host by cloaking itself in these fat-rich structures."

Understanding host lipid transport by Chlamydiae may have further implication for chronic infections, the researchers say. For example, lipid-rich macrophages ("foam cells") are a symptom in chlamydial pneumonia. Because foam cells are a key element in development of atherosclerosis, lipid droplet co-option also suggests a possible explanation for the association between chlamydial infections and heart disease.


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Source:American Society for Cell Biology


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