Scientists have explained via a model, how human immune system keeps at bay from TB.
The new tissue culture model using human white blood cells shows that people with a latent, or symptom-free, tuberculosis infection are protected from active disease by a critical early step in their immune response.
The model also shows, however, that some TB bacteria can find a way to get around that protection, which helps explain how latent infections turn into active and transmissible disease.
Senior author of the study, professor Larry Schlesinger at the Ohio State Universitym said that recent discovery of latent infections in Kansas schoolchildren who had contact with a single actively ill patient shows how widespread infection can occur with minimal exposure.
This research might help better in predicting what puts people with latent infection at higher risk of later developing active disease, he added.
In the study, scientists used human cells to create a model of a step in the immune response when immune cells gather together around a cluster of Mycobacterium tuberculosis cells, creating what is called a granuloma.
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The researchers created granuloma-like structures in cell cultures by adding TB bacterial cells to human white blood cell samples from people with and without latent TB infection. The cells from people with latent infection started forming large clusters as early as four days after infection, while cells from uninfected people took longer to produce smaller protective structures.
Compared to samples from uninfected people, the granuloma model containing immune cells from people with latent infection was a more effective fighter against bacteria in numerous ways: More immune cells were activated, and these cells controlled the bacterial load better. They also produced more protective proteins important to an immune response and were more capable of staving off the bacteria's efforts to use fatty acids and sugars for energy to help them grow.
But the study showed there is a downside to all of this heightened activity. Bacteria in these high-pressure immune environments were more likely to activate genes that let them adapt by changing their metabolism, giving the TB cells a place to thrive for the long term.
The model provided evidence that there was an immune response generated during latency that reduces Mycobacterium tuberculosis growth and thus was host protective, Schlesinger said.
The study is published in the journal mBio.