Let’s cover a topic that is rarely discussed in immunology – Silicosis. Have you ever imagined what happens when you breathe in silica?
Silica particles cause a severe condition called silicosis. As Ganesan et al. explain that silicosis is a fibrotic lung disease caused by the inhalation of respirable silica particles.
Where can we be exposed to silica particles?
Usually, exposure comes as a consequence of working with natural silica or silica-based artificial stones, however, it can also happen within the construction industry, mines, iron foundries, and quarries. According to American Lung Association, approximately 2 million construction workers and 300,000 workers in other industries are exposed to silica in the US. So, if you find your job description above, you should watch out! Why you might ask? Well, that brings me to the next question:
How serious is silicosis?
Unfortunately, very serious – the only treatment for terminal patients available is lung transplantation.
Now, that we understand the basics, let’s see how our immune system responds to silicosis:
When silica particles reach the alveoli, resident macrophages engulf the particles. These activated macrophages lead to the release of inflammatory cytokines. High inflammation levels will result in epithelium damage and progress to silicosis.
By comparing the immune samples from healthy people and patients diagnosed with silicosis, Ganesan et al. were able to notice some differences in the immune response:
1) Firstly, they analyzed proliferation. Both T cells and B cells from silicosis patients had higher proliferation when introduced to the silica particles in vitro compared to healthy controls. However, they did not see a certain elevation across T cell subsets.
2) Even though T cell subpopulations lacked in proliferation they were consistently more activated than the controls (remember that CD25 is the most prominent marker of cell activation!).
3) IgM and IgG antibodies were higher in silicosis patients compared to healthy individuals, with IgM at a much more significant extent. This points out the importance of B cells in silicosis.
4) Cells from silicosis patients made a higher number of aggregates which were also bigger in contrast to healthy cells.
5) In cases where stimulated patient cells and healthy cells did not differ in inflammatory phenotype, introducing more silica particles exploded inflammatory cytokine (IL-6, IL-1β, and TNF-α) responses from silicosis patients’ cells.
With this article, we now know these striking differences in immune responses from silicosis patients. As a concluding note, we could say that there is a different response to silica particles if the patient already suffers from silicosis. However, because this disease is so rare the sample size is considerably small. Does this mean we should not consider these results? Certainly not, but it does mean we require more research on silicosis.
Source:
Article author: Ines Poljak. Ines is a Ph.D. student at King’s College. She worked at the University of Copenhangen on multiple myeloma bone disease. She worked in several clinical laboratories before committing herself completely to research.
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