ECTRIMS eLearning

Air pollution as a novel contributor to the inflammatory activity of multiple sclerosis
Author(s): ,
S.M Villa
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia;Neurology Medical School, University of Siena, Siena
,
A Cortese
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
L Lova
Affiliations:
BD Bioscience, Milan;University of Pavia
,
P Comoli
Affiliations:
Pediatric Hematology/Oncology, IRCCS Policlinico S. Matteo
,
S La Salvia
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
G Nosari
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
G Mallucci
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
A Romani
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
D Franciotta
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
F Gigli Berzolari
Affiliations:
Department of Public Health, Experimental and Forensic Medicine, Unit of Biostatistics and Clininal Epidemiology, University of Pavia, Pavia
,
P Borrelli
Affiliations:
Department of Public Health, Experimental and Forensic Medicine, Unit of Biostatistics and Clininal Epidemiology, University of Pavia, Pavia
,
E Volpe
Affiliations:
Neuroimmunology Unit, Santa Lucia Foundation, Rome
,
S Basso
Affiliations:
Pediatric Hematology/Oncology, IRCCS Policlinico S. Matteo
,
I Guido
Affiliations:
Pediatric Hematology/Oncology, IRCCS Policlinico S. Matteo
,
G Quartuccio
Affiliations:
Pediatric Hematology/Oncology, IRCCS Policlinico S. Matteo
,
C Cereda
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
,
V Bollati
Affiliations:
Center of Molecular and Genetic Epidemiology, Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy
,
L Battistini
Affiliations:
Neuroimmunology Unit, Santa Lucia Foundation, Rome
R Bergamaschi
Affiliations:
Mondino National Neurological Institute of Pavia, Pavia
ECTRIMS Learn. Villa S. 09/14/16; 145530; EP1434
Silvia Maria Villa
Silvia Maria Villa
Contributions
Abstract

Abstract: EP1434

Type: ePoster

Abstract Category: Pathology and pathogenesis of MS - Environmental risk factors

Incidence of Multiple Sclerosis (MS) varies greatly with geographical location, being higher in western countries. Environmental air pollution has been associated with increased incidence and exacerbation of numerous respiratory, cardiovascular and rheumatologic diseases; however, little is known about the impact of air pollution on MS course. Here we investigated the relationship between air pollution, namely Particulate Matter 10 (PM10), and MS disease activity. 227 brain Magnetic Resonance Imaging (MRI), of which 77 (34%) showing contrast enhancing (CE) lesions, of 53 patients were considered. The mean PM10 level in 15 days prior MRI was significantly higher in patients with CE lesions compared with subjects without CE lesions (50,40 95%CI 44,70-56,26 vs 42,09 95%CI 38,47-45,60; f= 5,151, p=0,024), independently from time of the year, treatments and smoker-status. By Fluorescence-Activated Cell Sorting (FACS), we observed a significant correlation between mean PM10 levels and expression of CCR6 and PSGL1 on CD4+ and CD8+ T cells and LFA1 on CD4+ T cells. Moreover, in vitro treatment of Peripheral Blood Mononuclear Cells (PBMCs) with urban particulate matter led to increased expression of LFA1 and CCR6. Finally, urban particulate matter strongly induced secretion by monocyte derived Dendritic Cells (mdDCs) of Th17 polarizing IL6 and IL23 and, in mixed mdDC/PBMC cultures enhanced generation of IL17-producing T cells. We speculate that PM10 exposure in the lung may lead to MS exacerbation by inducing the production of autoreactive Th17 lymphocytes and by boosting their migratory capacity through the blood-brain barrier.

Disclosure: S. Villa: nothing to disclose

A. Cortese: nothing to disclose

L. Lova: nothing to disclose

P. Comoli: nothing to disclose

S. LaSalvia: nothing to disclose

G. Nosari: nothing to disclose

G. Mallucci: nothing to disclose

A. Romani: nothing to disclose

D. Franciotta: nothing to disclose

F. Gigli Berzolari: nothing to disclose

P. Borrelli: nothing to disclose

E. Volpe: nothing to disclose

S. Basso: nothing to disclose

I. Guido: nothing to disclose

G. Quartuccio: nothing to disclose

C. Cereda: nothing to disclose

V. Bollati: nothing to disclose

L. Battistini: nothing to disclose

R. Bergamaschi: nothing to disclose

Abstract: EP1434

Type: ePoster

Abstract Category: Pathology and pathogenesis of MS - Environmental risk factors

Incidence of Multiple Sclerosis (MS) varies greatly with geographical location, being higher in western countries. Environmental air pollution has been associated with increased incidence and exacerbation of numerous respiratory, cardiovascular and rheumatologic diseases; however, little is known about the impact of air pollution on MS course. Here we investigated the relationship between air pollution, namely Particulate Matter 10 (PM10), and MS disease activity. 227 brain Magnetic Resonance Imaging (MRI), of which 77 (34%) showing contrast enhancing (CE) lesions, of 53 patients were considered. The mean PM10 level in 15 days prior MRI was significantly higher in patients with CE lesions compared with subjects without CE lesions (50,40 95%CI 44,70-56,26 vs 42,09 95%CI 38,47-45,60; f= 5,151, p=0,024), independently from time of the year, treatments and smoker-status. By Fluorescence-Activated Cell Sorting (FACS), we observed a significant correlation between mean PM10 levels and expression of CCR6 and PSGL1 on CD4+ and CD8+ T cells and LFA1 on CD4+ T cells. Moreover, in vitro treatment of Peripheral Blood Mononuclear Cells (PBMCs) with urban particulate matter led to increased expression of LFA1 and CCR6. Finally, urban particulate matter strongly induced secretion by monocyte derived Dendritic Cells (mdDCs) of Th17 polarizing IL6 and IL23 and, in mixed mdDC/PBMC cultures enhanced generation of IL17-producing T cells. We speculate that PM10 exposure in the lung may lead to MS exacerbation by inducing the production of autoreactive Th17 lymphocytes and by boosting their migratory capacity through the blood-brain barrier.

Disclosure: S. Villa: nothing to disclose

A. Cortese: nothing to disclose

L. Lova: nothing to disclose

P. Comoli: nothing to disclose

S. LaSalvia: nothing to disclose

G. Nosari: nothing to disclose

G. Mallucci: nothing to disclose

A. Romani: nothing to disclose

D. Franciotta: nothing to disclose

F. Gigli Berzolari: nothing to disclose

P. Borrelli: nothing to disclose

E. Volpe: nothing to disclose

S. Basso: nothing to disclose

I. Guido: nothing to disclose

G. Quartuccio: nothing to disclose

C. Cereda: nothing to disclose

V. Bollati: nothing to disclose

L. Battistini: nothing to disclose

R. Bergamaschi: nothing to disclose

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