Air Pollution, Once Inhaled, Seen to Trigger Inflammation in RRMS Patients

Air Pollution, Once Inhaled, Seen to Trigger Inflammation in RRMS Patients
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Exposure to air pollution, particularly to particulate matter 10 (PM10), small airborne and inhalable particles, may trigger inflammatory reactions in people with multiple sclerosis (MS), an Italian study reported.

The study “Air pollution as a contributor to the inflammatory activity of multiple sclerosis” was published in the Journal of Neuroinflammation.

Previous studies have suggested a link between air pollution and relapses in MS, and possibly in other neurological disorders. Air pollution is increasingly seen as a risk factor for MS, as it promotes its inflammation. However, only a few studies have looked for possible links between air pollutants and relapses.

A team led by researchers in Italy, which conducted an earlier study, investigated further the effects of exposure to PM10  on inflammatory processes of MS.

This analysis involved 57 relapsing-remitting MS patients (mean age, 43) and 19 healthy people serving as controls (mean age, 46) to determine exposure to PM10 according to area of residence (all lived in Pavia, a province in northern Italy). The team assessed several inflammatory markers on circulating CD4 and CD8 T-cells, immune cells involved in MS development.

Results showed that higher exposure to PM10 was significantly associated with higher levels of the marker C-C chemokine receptor 6 (CCR6) on T-cells of MS patients. CCR6 are receptors for cytokines, molecules that aid communication between cells, and are characteristic of Th17 cells — cells that are important mediators of the immune response.

Of note, CCR6 is known to mediate early recruitment of Th17 cells to the central nervous system (CNS, the brain and spinal cord), where damage they can cause is considered a key step in MS development.

This finding suggests that PM10 exposure facilitates the migration of T-cells to the CNS by producing CCR6. No similar association between CCR6 levels and mean PM10 exposure was seen in healthy individuals.

In vitro studies confirmed the effects of PM10 exposure on the expression of CCR6 in peripheral blood mononuclear cells (PBMCs), a blood cell group that includes lymphocytes and dendritic cells. Higher level of CCR6 with increasing PM10 levels were also observed on PBMCs.

The team also assessed the effect of PM10 on cytokine production by monocyte-derived dendritic cells — important cells of the immune system that act as sentinels and can trigger an immune response.

Data showed that cytokine production — particularly IL1 beta, IL6, and IL23 — was significantly increased. “These cytokines are necessary for differentiation of Th17 into fully pathogenic cells,” the researchers wrote.

Based on these results, the team proposed that dendritic cells present in the lungs may catch PM10 and trigger an inflammatory response.  Th17 cells are then produced, and their ability to migrate into the CNS increases, leading to inflammatory exacerbations of the disease.

“We speculate that in MS respiratory exposure to PM10 may induce the production in the lung of autoreactive Th17 lymphocytes and boost their migratory properties,” the researchers wrote.

Nonetheless, “larger prospective studies are needed to confirm the effect of PM10 on Th17 cell polarization [differentiation into pathogenic, or disease-causing, cells] in MS patients, as well as to confirm the effect of PM10 on migratory properties of circulating [T-cells],” they added.

Further studies are also needed to determine if the inflammatory effect of PM10 is specific for MS, or can also be seen in other autoimmune diseases.

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Patrícia holds her PhD in Medical Microbiology and Infectious Diseases from the Leiden University Medical Center in Leiden, The Netherlands. She has studied Applied Biology at Universidade do Minho and was a postdoctoral research fellow at Instituto de Medicina Molecular in Lisbon, Portugal. Her work has been focused on molecular genetic traits of infectious agents such as viruses and parasites.

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