Ema Kantorova

Ema Kantorova

Comenius University Bratislava, Slovakia

Title: Role of adipokines in immune-mediated disorders of central nervous system including multiple sclerosis


Ema Kantorova's specialization is neurology and she finished PhD study last year (2011) and now she is a teacher, an Assistant Professor and postdoctoral fellow of the Jessenius Faculty of Medicine Comenius University in Martin. She studied medicine in Faculty of Medicine in Palacky University, Czech Republic. She live and work in Slovakia, Martin.


Introduction: Immune-mediated disorders of central nervous system (CNS) have experienced a dramatic increase in industrialized countries. Multiple sclerosis (MS) as a most common chronic disabling inflammatory-autoimmune demyelinating disease of the CNS affects genetically susceptible individuals. Epidemiological studies demonstrate that genetic susceptibility interacts with lifestyle and environmental and immunological factors in determining the risk of developing autoimmunity. Epidemiological observations have supported the role of vitamin D, sunlight exposure (encouraging endogenous production of vitamin D), the role of several infectious agents, socioeconomic status, smoking and environmental pollutants in determining the risk of developing autoimmunity, including MS. Role of a diet and hormones as being potent modulators of MS risk have been also investigating. High rate of overweight and obesity in population have awakened the interest of understanding a role of adipose tissue and adipokines as novel biomarkers or autoimmune disorders of central nervous system. The link between adipose-tissues-released factors and immune-mediated autoimmune disorders require high degree of suspicion. The white adipose tissue, long regarded as an inert energy storage tissue, has been recognized to be an essential endocrine organ, secreting a wide variety of soluble mediators termed “adipokines”. Adipokines previously associated with atherosclerosis, vascular pathology, metabolic syndrome, and risk of cardiovascular and cerebrovascular disorders have been implicated in innate and aquired immune processes both in animals and humans. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified. Among them leptin, adiponectine, resistin and visfatin belong to the most frequently evaluated adipokines. Material and methods: In our study we targeted relationship between adipokines (leptin and adiponectine), excess of adipose-tissue mass, and lipids (cholesterol and triglycerides) with disease activity in mutliple sclerosis pacients. The information was enriched with genetic background of examined patients. Presence of both HLA antigen DQB1a, 1b and HLA antigen DRB1 together with single nucleotid polymorphism rs 3135388, strongly specific markers of genetic succesability ro MS, were involved into analyses. Total of 74 patients (60 female, 14 male) completed the study. The mean age in the group was 40.8±10.5, disease duration 11.1 ±4.8. Rate of disability was 3.7±1.4 (range 0-10) (measured by Kurtzke "expanded disability status scale" (EDSS). Higher EDSS corresponds with more pronounced disability. Body mass index (BMI) was used to evaluate adipose-tissue-mass, mean value was 25.3±5.6. Cholesterol and triglyceride plasma levels were noted. Leptin and adiponectin were tested ELISA method (Biovendor). Statistical analysis included nonparametric Kendall-tau b test. Results: We found significant association of higher leptin with higher EDSS (r=0.22, p=0.006), and lower adiponectin with higher EDSS (r=- 0.17, p=0.036). Both leptin and adiponectin were associated with BMI. But only lower adiponectin, not leptin, correlated with the carriage of HLADRB1 and rs 3135388 A (r=0.16, p=0.053), conferring a threefold higher risk of multiple sclerosis. However hypercholesterolemia, reported as most common comorbidity in MS, also strongly correlated with HLADRB1 (r=0.17, p=0.031), and rs3135388 (r=0.21, p=0.01). Conclusion: Both lower adiponectin and higher leptin correlated with severer disease disabilit in multiple sclerosis patients. We concluded obesity as being the potential important epigenetic factor in MS pathogenesis. Adiponectin, more than leptin is associated with genetic susceptibility resulting in neurological disability in MS patients. Hypercholesterolemia is also associated with genetic susceptibility to multiple sclerosis. Precise role of adipokines in immune processes contributing into MS pathogenesis require future studies.