The Nottingham Covid Research Group is led by Professor Gisli Jenkins from the University of Nottingham

Professor Jenkins group has been working on understanding the role of the alveolar epithelium in the pathogenesis of pulmonary fibrosis for nearly 20 years, and it is the alveolar epithelium that is damaged in severe Covid-19. Therefore, we have refocused our efforts on understanding three key aspects of how alveolar damage occurs in following SARS-CoV-2 infection based on what is currently known about the SARS-CoV-2 receptor ACE2.

ACE2 is expressed on a wide range of epithelial cells, most notably in the upper airways, kidney, and gut which might explain a number of the symptoms (Cough, changes in sense of smell, diarrhoea and renal failure), surprisingly however levels of ACE2 are low in the normal alveolar epithelium suggesting that ARDS is either a) not a direct consequence of alveolar infection by SARS-CoV-2 but due to a ‘cytokine storm’, b) that comorbidities such as heart disease, diabetes, high blood pressure or chronic lung disease alter the ACE2 expression in the alveoli or c) another receptor is required to facilitate cell entry of the SARS-CoV-2 virus in the alveoli.

Furthermore, ACE2 can also exist as a soluble molecule and high levels can be found in the blood of people with Diabetes and Hypertension who are at increased risk of severe Covid-19. However, whether soluble ACE2 facilitates viral entry to the alveolar epithelium or acts as a decoy receptor and reduces viral entry to the alveolar epithelium is not known.

The focus of the Nottingham Covid Research Group

  1. Define whether SARS-CoV-2 gains entry to alveolar epithelium using a second receptor (eg Integrins) as well as, or instead of ACE2.

  2. Determine whether soluble ACE2 facilitates, or inhibits alveolar uptake of SARS-CoV-2.

  3. Determine the expression levels of ACE2 and potential co-receptors (eg integrins) in the alveoli in a range of diseases at various times throughout the life course.

  4. Review the evidence that drugs which have the potential to protect the alveoli from a ‘cytokine’ storm might be useful therapies for severe Covid disease.

  5. Determine the long term consequences of alveolar damage in Covid-19 related ARDS on the development of progressive pulmonary fibrosis.


To help facilitate rapid breakthroughs we will post more details relating to each of these goals as and when have the protocols and preliminary data available so others can:


  • a) provide feedback

  • b) replicate

  • c) collaborate with us on these studies.

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