Speaker Biography

Ivana Haluskova Balter

French society of immunology, France

Title: Neurodegenerative diseases & role of microbiota and immune system

Ivana Haluskova Balter

Haluskova Balter Ivana, active medical professional specialised in infectious diseases, internal medicine covering various therapeutic axes, certified in Immunology and Pediatric, MBA in vaccinology and years of clinical practise contributing to bring innovative science and diplomacy for global health (Switzerland) and most importantly to set up intelligent partnership borderless. Lived multi-country medical “field “experience in Southeast Asia, West/Central/East Europe and Middle East. Over 15 years of experience in pharmaceutical research and development for European and USA companies as Medical lead /Director of R&D in various therapeutic areas and as Scientific and Medical independent consultant for various stakeholders globally. Active as speaker on various congresses to bring science to clinic, member of French immunology society (SFI) administrative board and several international academic societies (focus on innovation of R&D reflecting immunology and genetic variability, role of immunologic approach for treatment and diagnostic, tackle problem of resistance for antimicrobials, antimalarial, antivirals etc). Member of advisory Health concern (India) and think tank group in order to attract attention to role of accessible medical care, education and awareness along with accurate diagnostic and innovative partnership in this area. Years of expertise to work globally but recently more focused on France and BRICs and Asia (India and Russia in particular) as Medical advisor for scientific partnership, bringing new innovative concepts alive and getting them endorsed.


The gut-brain axis  consists of bidirectional communication between the central and the enteric nervous system, linking emotional and cognitive centers of the brain with peripheral intestinal functions. This interaction between microbiota  appears to be bidirectional, namely through signaling from gut-microbiota to brain and from brain to gut-microbiota by means of neural, endocrine, immune, and humoral links. It is already well known that interactions between the immune and nervous systems play an important role in modulating host susceptibility and resistance to inflammatory disease. Neuroendocrine regulation of inflammatory and immune responses and disease occurs at multiple levels.  While many genes and environmental factors contribute to susceptibility and resistance to autoimmune/inflammatory diseases, a full understanding of the molecular effects on immune responses of combinations of neuropeptides, neurohormones and neurotransmitters at all levels has opened up new therapeutic approaches and are essential for the design of future therapies based on such principles. Influence of our microbiota on immunity and metabolism, more recent researches  suggest that microbes impact many different brain functions and could be potentially involved in several neuropathologies including neurodegenerative diseases like sclerosis multiplex and Alzheimer’s disease(AD). Bacteria populating the gut microbiota can secrete large amounts of amyloids and lipopolysaccharides, which might contribute to the modulation of signaling pathways and the production of proinflammatory cytokines associated with the pathogenesis of AD. Imbalances in the gut microbiota can induce inflammation that is associated also with the pathogenesis of obesity, type 2 diabetes mellitus, and Alzheimer’s disease. Studies using experimental models have indicated that multiple sclerosis (MS)-like disease can be triggered in the gut following interactions of brain autoimmune T lymphocytes with local microbiota and recent results offer functional evidence that human microbiome components contribute to CNS-specific autoimmunity. evidence that human MS-derived microbiota contain factors that precipitate an MS-like autoimmune disease in a humanized transgenic mouse model. This observation provides possibilities for characterizing the precise role and functional mechanisms by which the human intestinal microbiota contributes to the pathogenesis of neuroinflammatory diseases. The findings may eventually have important implications not only for the pathogenesis but also for the therapy and potentially even prevention of human MS. Futher research moving forward to see potential intervention knowing that modulation of the gut microbiota might be one promising therapy for MS. Oral treatment with ECN(Escherichia coli strain Nissle 1917), but not with the archetypal K12 E. coli strain MG1655, reduced the severity of EAE (experimental autoimmune encephalomyelitis). This beneficial effect was associated with a decreased secretion of inflammatory cytokines and an increased production of the anti-inflammatory cytokine IL-10 by autoreactive CD4 T cells, both in peripheral lymph nodes and CNS. Interestingly, ECN-treated mice exhibited increased numbers of MOG-specific CD4+ T cells in the periphery contrasting with severely reduced numbers in the CNS, suggesting that ECN might affect T cell migration from the periphery to the CNS through a modulation of their activation and/or differentiation. In addition, we demonstrated that EAE is associated with a profound defect in the intestinal barrier function and that treatment with ECN. Futher research to explore diagnosis and treatment of CNS diseases and link with human microbiota and crosslinks with immune system and CNS translated to innovative approaches promise to bring innovative solutions for patients benefit.