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Jean-Eric Ghia MSc, PhD, HDR

Currently Not Accepting Students.

Current Position

Assistant Professor in Department of Immunology, and Department of Internal Medicine section of Gastroneterology, University of Manitoba; Researcher, Children’s Hospital Research Institute of Manitoba; Director of the Gastrointestinal Basic Biology Research at the Inflammatory Bowel Disease Clinical & Research Centre, University of Manitoba

Research Focus

Inflammatory bowel disease (IBD) are idiopathic, chronic intestinal disorders of complex pathogenesis and involve an aberrant immune response to some environmental antigen in genetically predisposed adults and children. Current treatments for IBD address the symptoms and are not curative, and they have potentially serious side effects. Thus, new, effective and safer therapies are required.

The primary mission of my laboratory is to develop novel therapeutic strategies in this field. My research interests have mainly been in the areas of neuroinflammatory mechanisms and neuroendocrine peptides. I have extensive research training at world-renowned institutes. Building upon my expertise in gut neuro-inflammation, my laboratory is exploring the role of neuroimmunoendocrine regulation during the development of gastrointestinal inflammation and is elucidating the mechanisms involved in the evolution of the gut maintaining its normal immune homeostasis to developing chronic gastrointestinal inflammatory disease.

Our research is divided in four novel innovative programs:

  1. i) Our first goal is to further explore the brain-gut axis and define more precisely the gut immunologic response during the development of depressive-like behaviour. We are also exploring the implication of the vagus nerve in the context of colitis.

The goal of this innovative and high impact study is to demonstrate that the widespread use and potential impact of neural modulation (e.g. use of anti-depressant and pharmacological stimulation of the vagus nerve) may be important therapeutic adjuncts to the conventional approach in IBD.

  1. ii) The second goal is to explore the use of chromogranin-A (CgA)-derived peptides as markers or as a therapeutic treatment in the prevention of chronic quiescent colitis, an approaches not present in or outside Canada. We anticipate this research will lead to the development of new diagnostic markers in IBD and possibly new treatments

iii) Third, semaphorin 3E (Sema3E) has emerged as an new essential axis involved in the dendritic cell immunoinflammatory response; however, the role of Sema3E in IBD is unknown and we will continue to explore its role in the context of chronic quiescent colitis and in IBD. Our data demonstrated that Sema3E could be a protein of interest in developing new treatments for patients with IBD.

  1. iv) External factors during pregnancy may influence the future development and behavior of the infant. The use of antibiotics during pregnancy or around the time of delivery is a common practice in clinical settings, more so because of the fear of newborn colonization with Group B streptococci (GBS) during passage through the birth canal or when the membranes rupture. Perinatal antibiotics may influence the initial microbial colonization of the newborn intestine, which is essential for normal host development, and the early neonatal period represents the most important opportunity for microbiota-induced host-homeostasis . The use of broad-spectrum antibiotics in the perinatal period has been shown to alter the expression of genes involved in gastrointestinal tract development, with major consequences on the architecture and functionality of the intestinal barrier. Moreover, antibiotics given to pregnant mothers in the days before delivery have been shown to significantly alter the composition of the preterm newborn microbiota, reducing intestinal microbial diversity on the first stool samples. The rapid increase in illnesses that have their onset in childhood (including asthma, allergies, type 1 diabetes, obesity and autism) suggests that an environmental cause could be present, and the loss of one or more constituents of the indigenous microbiota after maternal antibiotic exposure could be a contributing factor. In addition, perinatal antibiotic-mediated microbiota disturbances may increase the risk for late-onset sepsis and necrotizing enterocolitis, which may constitute life threatening risks for preterm newborns. Despite the high association between the impact of perinatal or neonatal antibiotic use on the microbial colonization and the future risk for asthma, other allergic reactions and other disease conditions, the effects of perinatal antibiotic use on the process of intestinal microbiota development and future susceptibility to IBD remain elusive or poorly understood. The aim of our research are to assess the susceptibility to colitis and composition of colonic and fecal microbiota and functional alterations in mice that were exposed to perinatal antibiotics and treated experimentally to induce acute colitis later in life.

All four studies are highly novel as they will not only demonstrate the role of new drugs or proteins of interest in animal models of colitis, but in a translational perspective, using clinical samples, they will expand their roles in the clinical context of IBD.