Andrew Masterson
Andrew Masterson is a former editor of Cosmos.
Silicosis – a type of lung disease caused by the inhalation of crystalline dust – may be an ancient legacy bequeathed to humans by our extremely distant ancestors, marine sponges.
That’s the surprising conclusion reached by a team of researchers led by Marina Pozzolini of the University of Genova, Italy, and published in the Journal of Experimental Biology.
Pozzolini and her colleagues launched their enquiry after noting that marine sponges of the species Chondrosia reniformis were able to absorb silica grains and use them in a way that was beneficial – in very stark contrast to what happens when they enter human lungs.
Despite an overall improvement in workplace health and safety, silicosis still kills more than 9000 people around the world each year.
The disease arises when fine silica dust enters the lungs. Its presence prompts the body to produce excess collagen fibres and large amounts of a protein called tumour necrosis factor (TNF), which causes inflammation.
Exposing marine sponges to fine quartz dust, Pozzolini and her colleagues noted that exactly the same things were happening: the animals absorbed the crystal while producing large amounts of collagen and TNF.
The end result, however, was radically different. The sponges incorporated the crystal dust and the collagen into their bodies, bolstering their strength and stiffness.
The observation led to the idea that perhaps the genetic code for production of TNF – strongly conserved for hundreds of millions of years and therefore present across the animal kingdom – might be linked to the way tissues respond to silica dust.
The ability to produce TNF is largely beneficial for humans: it plays a critical role in regulating the immune system. Pozzolini’s team, however, suggest that TNF production is intimately tied up with reactions to silica dust – a process that was clearly beneficial in our sponge ancestors, but decidedly not in the case of more complex animals.
“Thus,” the team conclude, “we put forward the hypothesis that an ancient physiological behaviour from the lowest of the Metazoa, persisting through evolution via the same molecular mediators such as TNF, may have become the cause of disease in the specialised tissues of higher animals such as mammals.”
