New advance made in TB research
July 30th, 2010 - 5:33 pm ICT by ANIWashington, July 30 (ANI): Existing drugs can potentially target tuberculosis’ ability to spread, according to a McGill University researcher.
“It’s a global health disaster waiting to happen, even here in Canada, but this new paradigm in TB research may offer an immediate opportunity to improve vaccination and treatment initiatives,” said Dr. Maziar Divangahi of the Research Institute of the McGill University Health Centre.
The ability of TB bacteria to persist in individuals with apparently normal immune systems implies that they have developed strategies to avoid, evade, and even subvert immunity. The bacteria mainly enter the body through inhalation into the respiratory tract. Alveolar macrophages, a type of white blood cell residing in our lungs, initially recognize the bacteria and engulf them. This process is one of our immune system’s defence mechanisms. However, TB has evolved into a parasite that can survive and replicate inside the macrophages until they burst out, spreading the infection.
The way infected macrophages die is a determining factor in the development of immunity to TB. Macrophages can induce apoptosis, a type of cell death which keeps their membrane intact, trapping and reducing bacterial viability. However, TB bacteria induce another type of cell death called necrosis. Necrosis causes cell death by disrupting the cell membranes, which enables the bacteria to escape the cell. It may help to visualize a box with broken walls.
The key to the fate of the macrophages is the balance between two kinds of eicosanoids. Eicosanoids are molecules that contribute to the control of our immune system. The genetic code of TB bacteria enables it to tip this balance in favor of necrosis, and human genetic analysis revealed that modification in eicosanoids production is associated with susceptibility or resistance to TB. Fortunately, drugs that target the production of eicosanoids are already in use for treating other inflammatory diseases, such as rheumatoid arthritis.
“The next steps will be to see exactly how these drugs can be used to treat TB,” said Divangahi. (ANI)
- New findings on drug tolerance could help cure TB faster - Mar 04, 2011
- New dual recognition mechanism found in TB - Sep 10, 2010
- How TB bacteria to survive in infected organs - Dec 07, 2010
- Ciggie smoke 'weakens lungs' natural defense against harmful pathogen' - Oct 24, 2009
- Novel approach shows great potential in reducing mortality from flu - Apr 23, 2011
- Scientists find promising new TB vaccine candidate - Mar 19, 2011
- Clues to how bacteria and viruses are identified as enemies revealed - Oct 01, 2010
- Unexpected find may lead to novel ways to stop HIV - Jan 24, 2011
- Scientists find TB disease mechanism along with compound to block it - Feb 16, 2010
- Study shows experimental immune-boosting drug worsens TB in mice - Apr 13, 2010
- New signaling pathway linked to inflammatory disease discovered - Dec 15, 2010
- Naturally occuring protein reverses brain damage caused by meningitis - Jun 11, 2010
- Protein knocks out HIV by starving it of raw materials - Feb 13, 2012
- New cell type boosts immunity to infection - Nov 30, 2011
- Immune system can abort stem cell regeneration - Nov 21, 2011
Tags: alveolar macrophages, broken walls, cell death, cell membranes, defence mechanisms, genetic analysis, genetic code, health disaster, inflammatory diseases, maziar, mcgill university health, mcgill university health centre, new paradigm, target, tb bacteria, tb research, treatment initiatives, university health centre, university researcher, white blood cell