How is tuberculosis immunity altered by household air pollution TB-HAP

  • Research type

    Research Study

  • Full title

    Alveolar macrophage/Mycobacterium tuberculosis interaction in the real world: the influence of environmental particles on drug action and macrophage killing (the TB-HAP study)

  • IRAS ID

    177610

  • Contact name

    Jamie Rylance

  • Contact email

    jrylance@liv.ac.uk

  • Duration of Study in the UK

    1 years, 11 months, 30 days

  • Research summary

    Current evidence suggests an independent association between two major co-existent global health problems: tuberculosis (TB) and household air pollution (HAP). HAP is the 3rd biggest risk factor for ill-health worldwide, and results from people using open fires to cook, light and heat their homes.

    HAP impairs immune defence in the lung by compromising the ability of the alveolar macrophage (a key front-line immune cell) to take up tuberculosis causing bacteria, and to kill them effectively.

    Even with the best TB control programmes in the developing world, there is a 20% treatment failure rate. There may be many reasons for this, but we suggest that HAP is likely to contribute particularly because the parts of the world with high rates of TB also have high rates of HAP.

    We want to examine how the alveolar macrophage cells are altered when then are exposed to smoke particles, and how this affects tuberculosis killing. The most reliable results will come from using human cells, and we would like to obtain cells using a telescope test to wash them out from the lungs of healthy volunteers (bronchoscopy).

    We will use the cells in the laboratory to look at how the anti-bacterial action is altered when we apply smoke particles. We will examine a number of mechanisms which might be affected, including how well the immune cells cause inflammation and how well the cells take up and sterilise the tuberculosis.

    This is important because current tuberculosis drug development assumes that immune cells are perfectly functional. Our drug model may therefore be flawed. This research may in future help to identify people with high risk of treatment failure, and prompt alternative therapy.

  • REC name

    North West - Preston Research Ethics Committee

  • REC reference

    15/NW/0289

  • Date of REC Opinion

    30 Apr 2015

  • REC opinion

    Favourable Opinion