Cystic fibrosis (CF) is an inherited genetic condition that affects around 10,000 people in the UK. Caused by a mutation in the CFTR gene, CF is typified by incorrect transport of salt and water into and out of cells, which leads to the production of thick, sticky mucus in the digestive system and lungs.
Due to the presence of excess mucus, people with CF are at risk of frequent lung infections. One of the most common bacterial species involved in these infections is Pseudomonas aeruginosa, which can be difficult to treat and carries an increasing risk of antibiotic resistance.
In order to better understand how P. aeruginosa is able to colonise lung tissue, researchers at the University of Nottingham have turned to an unusual source: a local butcher. Specifically, the group worked with the Nottingham butcher JT Beedham & Sons, who provided them with pigs’ lungs that they could then use to grow the P. aeruginosa bacteria.
Warning: This video contains images of pig innards.
Using these lungs as a model for disease has a number of advantages: structurally and immunologically they are similar to human lungs; and, importantly, they are post-consumer waste. By finding another use for the lungs, researchers can reduce the number of animals that need to be used in CF research.
Dr Freya Harrison, who led the research (and appears in our video) explained what the group are able to study by using the pig lungs: “We’re able to monitor the progress of the P. aeruginosa infection and study how the bacteria evolve and diversify.
“We found that our pig lung model also made it easier for us to study the cell-to-cell interactions in the bacterial population, a phenomenon called ‘quorum sensing’, which is the target of new pharmaceutical research to fight antibiotic-resistant infection.”
You can find more information about Freya’s work and the work of the group that she’s part of here.
Harrison, F., Muruli, A., Higgins, S., & Diggle, S. (2014). Development of an Ex Vivo Porcine Lung Model for Studying Growth, Virulence, and Signaling of Pseudomonas aeruginosa. Infection and Immunity, 82 (8), 3312-3323 DOI: 10.1128/IAI.01554-14