particolato atmosferico

Autoimmune Diseases and Smog: New Risk Factor for Rheumatoid Arthritis Discovered

A new study coordinated by the Sapienza Department of Internal Medicine and Medical Specialities has experimentally revealed the role of particulate matter air pollution in the development of autoimmune diseases such as rheumatoid arthritis. The results of the study have been published on Cell Death & Disease.

An increasing body of scientific evidence indicates that environmental factors may contribute to the pathogenesis of autoimmune diseases, especially those of the rheumatoid type. Proving the role of environmental pollution in the insurgence of these pathologies not only increases they risk factors, but also extends the fields for action and prevention.

This is the very context in which the research study coordinated by Professor Guido Valesini from the Sapienza Department of Internal Medicine and Medical Specialities, in collaboration with Silvana Fiorito and researchers at the Translational Pharmacology Institute (IFT) and the National Research Council (CNR), was recently published on Cell Death & Disease. The study focuses on the role of particulate matter air pollution produced by the combustion of gasses in Euro 4 and Euro 5 diesel motors and evaluated its effects on the functionality and biological characteristics of bronchial cell tissues.

The results revealed how soot nanoparticles (one of the main components created by diesel motor combustion) can induce autophagy (a form of self-digestion) and death by apoptosis of cells in the bronchial epithelium and concomitantly produce “citrullinated” proteins.

“It is interesting to underline,” points out Prof. Valesini, “how Euro 5 particulate is potentially more damaging that that produced by Euro 4 motors. This demonstrates that a reduction in the quantity of particulate emissions does not automatically translate into a reduction of the toxic effects.” Citrullination is a natural and physiological process that regulates protein functions. However, in patients suffering from rheumatoid arthritis, this process becomes excessive and provokes a pathological accumulation of citrullinated proteins. These, in turn, cause an immunological response that produces antibodies directed against these proteins, leading to an autoimmune attack on normal tissues.

It has already been demonstrated that an increase in citrullination levels is correlated to a greater risk of developing Rheumatoid Arthritis. Indeed, in order to diagnose this condition, one of the tests reveals the antibodies directed against citrullinated proteins (ACPA). “On the basis of our observations,” explains Prof. Valesini, “we can hypothesise that atmospheric pollution may play a non-secondary role, in subjects predisposed and through complex mechanisms, in the pathogenesis of some immune-mediated diseases such as rheumatoid arthritis.”

We currently do not know the main cause of the pathology, however the studies that point to environmental factors as a co-cause are increasingly gaining credit. Currently, the main environmental factor that is known to induce the cellular exposition of citrullinated proteins is cigarette smoke. The research team hunted down other factors that may induce the production of citrullinated proteins and activate the immune system, revealing how smog plays a crucial role in this.

Particulate is one of the greatest pollution factors in urban areas and an important risk factor for chronic inflammatory pathologies. Addressing risk factors and basing the development of public health policy around them is fundamental to extend our life expectancy and guaranteeing the quality of our lives.

 

References:

Diesel exhaust particles induce autophagy and citrullination in Normal Human Bronchial Epithelial cells - Tania Colasanti, Silvana Fiorito, Cristiano Alessandri, Annalucia Serafino, Federica Andreola, Cristiana Barbati, Francesca Morello, Michela Alfè, Gabriele Di Blasio, Valentina Gargiulo, Marta Vomero, Fabrizio Conti and Guido Valesini - Cell Death & Disease (2018) 9:1073. DOI 10.1038/s41419-018-1111-y

 

For further information

Guido Valesini
Department of Internal Medicine and Medical Specialities, Sapienza University 
Tel. (+39) 0649974631 
guido.valesini@uniroma1.it

 

Monday, 05 November 2018

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