Study identifies immune response that enables TB bacteria to multiply, provides new target for TB drugs

Researchers have identified an immune system response to tuberculosis that enables TB bacteria to spread through the lungs, providing a new target for TB drug development, according to a study published Sunday in Nature Immunology, AFP/Washington Times reports.

For the study, Heinz Remold of Brigham and Women's Hospital and researchers from Harvard Medical School examined immune system responses to TB bacteria in mice infected with cultured bacteria. The researchers found that when TB infects specialized immune cells in the lungs called macrophages, it turns the cells into incubators, allowing TB bacteria to multiply. When macrophages encounter weak strains of TB, the immune system triggers a self-destructive process called apoptosis, which keeps cell membranes intact and prevents TB bacteria from spreading (AFP/Washington Times, 9/15). Another biological mechanism then destroys the infected cell (Daily Mirror, 9/15).

However, the researchers found that more virulent TB strains suppressed apoptosis and triggered a process called necrosis, a type of cell death that allows TB bacteria to infect other cells (AFP/Washington Times, 9/15). Necrosis blocks the essential mechanism for apoptosis, preventing the formation of the protective membrane that destroys the infected cells (Herald, 9/15).

According to Remold, necrosis is "detrimental" because it "releases viable intercellular bacilli for spreading infection and promotes tissue damage" associated with advanced TB. The study's findings could provide a new target for TB drug development and encourage new strategies for fighting the disease by identifying the biochemical process that stimulates the formation of the protective membrane in apoptosis, AFP/Times reports (AFP/Washington Times, 9/15).

An abstract of the study is available online.