Extracellular Vesicles in the Pathogenesis of ARDS (VESPER)

  • Research type

    Research Study

  • Full title

    Investigating the role of Extracellular Vesicles in the Pathogenesis of Acute Respiratory Distress Syndrome (VESPER)

  • IRAS ID

    318757

  • Contact name

    Rahul Mahida

  • Contact email

    r.mahida@bham.ac.uk

  • Duration of Study in the UK

    4 years, 11 months, 30 days

  • Research summary

    When some people have a severe infection, their body's defence systems can over-react and damage their own organs through inflammation. In the lungs, we term this process Acute Respiratory Distress Syndrome (ARDS). ARDS causes the lungs to fill up with water, making it very difficult to breathe. These patients are looked after in the intensive care unit (ICU), where a machine can support their breathing. The death rate associated with this is 40%.

    Cells within the body can form outpouchings which break off to form extra-cellular vesicles (EVs). These EVs carry genetic material between different cell types and can affect how cells function.
    We know that lung defender cells (alveolar macrophages) in patients with ARDS do not work as well as in healthy people. Their ability to clear away dead cells is weakened, leading to increased inflammation, and risk of death. We want to determine whether transfer of genetic material by EVs to these defender cells may contribute to inflammation in ARDS.

    Seriously ill patients who require breathing machine support and who have sepsis (with or without ARDS) will be eligible for this study. Patients will be recruited from the ICU of the University Hospitals Birmingham NHS Trust. Study involvement will last up to 1 month for each patient. Participation in this study will not affect the clinical care that patients receive; however additional samples of blood, urine and lung washings will be taken for research purposes. These samples are also routinely taken as part of normal clinical care in the ICU.

    We will treat healthy defender cells with EVs derived from patient samples, to see if this reduces their ability to clear away dead cells. We will then determine what genetic material is transferred by the EVs, and whether preventing this will restore defender cell function and reduce inflammation.

  • REC name

    London - Brighton & Sussex Research Ethics Committee

  • REC reference

    22/LO/0872

  • Date of REC Opinion

    16 Dec 2022

  • REC opinion

    Further Information Favourable Opinion