Dr. Jean-Eric Ghia
 Dr. Jean-Eric Ghia

 - Associate Professor, Depts of Immunology & Internal Medicine (Section of Gastroenterology)
University of Manitoba
- Director, Gastrointestinal Basic Biology Research, IBD Clinical & Research Centre


- Habilitation (Accreditation to supervise research). Faculty of Health Sciences, University of Strasbourg, France
- Post-Doctorate Fellow,  McMaster University, Hamilton, Canada
- Ph.D. in Neurosciences, Faculty of Health Sciences, University of Strasbourg, France
- University diploma of clinical trials investigator (Postgraduate Degree), Faculty of Medicine, University of Strasbourg, France
- Control and quality assurance certificate. Transgène SA, Faculty of Medicine, University of Strasbourg, France
- Industrial and intellectual patent and law certificate, Faculty of Law, University of Strasbourg, France
- Postgraduate degree (DEA) in Neurosciences,  Faculty of Health Sciences, University of Strasbourg, France
- M.Sc. in Cellular Biology and Physiology, orientation: General Physiology and Pharmacology,  Faculty of Health Sciences, University of Strasbourg, France
- Bachelor of Biology and Physiology, orientation: Neurophysiology, Faculty of Health Sciences, University of Strasbourg, France

Mailing address

Department of Immunology
College of Medicine,
Faculty of Health Sciences
Room 431 Apotex Centre
750 McDermot Avenue
Winnipeg, Manitoba  R3E 0T5 

Tel: (204) 789-3802
Fax: (204) 789-3921
Email: Jean-Eric.Ghia@umanitoba.ca or  jeghia@yahoo.fr
Linkedin: tinyurl.com/nvudqt2
Pubmed: tinyurl.com/qyggbg4

Research Interests

Inflammatory bowel diseases (IBD) are chronic, relapsing intestinal disorders of complex pathogenesis, and including Crohn’s disease (CD) and ulcerative colitis (UC). IBD is the most common and serious chronic inflammatory condition of the gastrointestinal tract. The incidence of each disease is approximately 15/100,000 population in Canada. IBD is thought to arise secondary to a genetically determined susceptibility to inflammation triggered by unknown environmental factors. The most common course of disease is one of recurrent relapses. The disease and relapses include behavioural, neuroimmune, endocrine and enteric neuronal dysregulation, all of which may be interconnected. 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 vision of our program is to develop a better understanding of the pathogenesis of IBD and, in so doing, to develop new treatment paradigms that are both safer and more effective than current treatment options.

Specifically, our program direction is to tackle the above three major aspects of IBD pathogenesis in exploring the psychoneural immune underpinning of these diseases. Our centre has reported that depression may coincide with the emergence of IBD and may antedate its presentation by years. In IBD patients, there is an autonomic imbalance, with decreased parasympathetic function (i.e. vagus nerve tone (VN)). Our work and that of others has recently demonstrated that the immune system is regulated by depressive-like behaviour (DLB) and the VN. Therefore, one aim of our program is to define how DLB and VN regulate mucosal and mesenteric innate immune cells in colitis. We are exploring the extent to which psycho-interventions may be important therapeutic adjuncts to the conventional approach in IBD.

Colitis is associated with an alteration in enterochromaffin cells (EC). Chromogranin-A (CgA) of the granin family of proteins is stored in EC cells and gives rise to a peptide, catestatin (CTS), which has antimicrobial activity and regulates monocytes. Circulating CgA and CTS levels are elevated in IBD patients. A second aim is to define how CTS regulates gut physiology and colitis. This research is highly novel, and we expect it to lead to new diagnostic markers in IBD and to development of new antibacterial peptides. This research plan has great potential to generate economic activity through commercialization of the applications.

Finally, we identified a protein in the semaphorin (Sema) family that is implicated in the immune regulation of gut inflammation. Recently, semaphorin 3E (Sema3E) and its receptors plexinD1 (PLXD1) have emerged as an essential axis involved in dendritic cell (DC) immunoinflammatory responses, however, the role of Sema3E in IBD is not known. Our third aim is to determine the role of Sema3E in colitis. This study is highly novel as it will demonstrate the role of Sema3E in colitis and expand its role in the clinical context of IBD.

All three 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. To support these studies, we have developed collaborations with world-renowned scientific experts in Canada (Dr. Bernstein, University of Manitoba), United-States (Prof. Tracey), Iran (Dr. Dehpour) and France (Dr. Metz-Boutigue).

As the cause of IBD is not well understood, the elucidation of new regulatory pathways implicated in the IBD’s pathogenesis will have great potential in the development of new therapeutic strategies.


Ghia JE, Crenner F, Metz-Boutigue MH, Aunis D, Angel F. The effect of a chromogranin A-derived peptide (CgA4-16) in the writhing nociceptive response induced by acetic acid in rats. Life Sci. 2004; Aug 27, 75(15): 1787-99.

Ghia JE, Crenner F, Rohr S, Meyer C, Metz-Boutigue MH, Aunis D, Angel F. A role for chromogranin A (4-16), a vasostatin-derived peptide, on human colonic motility. An in vitro study. Regul. Pept. 2004; Sep 15, 121(1-3): 31-9.

Ghia JE, Crenner F, Metz-Boutigue MH, Aunis D, Angel F. Effects of a chromogranin-derived peptide (CgA 47-66) in the writhing nociceptive response induced by acetic acid in rats. Regul. Pept. 2004; Jul 15, 119(3): 199-207.

Ghia JE, Pradaud I, Crenner F, Metz-Boutigue MH, Aunis D, Angel F. Effect of acetic acid or trypsin application on rat colonic motility in vitro and modulation by two synthetic fragments of chromogranin A. Regul. Pept. 2005; Jan 15, 124(1-3): 27-35.

Ghia JE, Blennerhassett P, Verdu E, Ondiveeran KH, Collins SM. The vagus nerve: a tonic inhibitory influence associated with inflammatory bowel disease in a murine model. Gastroenterology 2006; Oct, 131(4): 1122-1130

Verma-Gandhu M, Verdu E, Bercik P, Blennerhassett P, Al-Mutawaly N, Ghia JE, Collins SM. Visceral pain perception is determined by the duration of colitis and associated neuropeptide expression in the mouse. Gut 2007; Mar, 56(3): 358-64

Ghia JE, Blennerhassett P, Collins SM. Vagal integrity and experimental colitis. Am. J. Physiol. 2007; Sep, 293(3): G500-507

Ghia JE, Blennerhassett P, El-Sharkawy RT and Collins SM. The protective effect of the vagus nerve in a murine model of chronic relapsing colitis. Am. J. Physiol. 2007; Oct, 293(4): G711-718

Motomura Y, Ghia JE, El-Sharkawy RT, McLaughlin J, Grencis RK, Collins M, Khan WI. Intestinal physiological changes and protective immunity to the same infectious agent differ in Th1 and Th2 dominant environments. Gut 2008; Apr, 57(4): 475-81

Ghia JE, Galeazzi F, Ford DC, Hogaboam CM, Vallance BA and Collins SM. Role of M-CSF dependent macrophages in colitis is driven by the nature of the inflammatory stimulus. Am. J. Physiol. 2008; Mar, 294(3): G770-777

Ghia JE, Blennerhassett P, Collins SM. Attenuation of colitis by tricyclic anti-depressant is mediated via the vagus nerve. J. Clin. Invest. 2008; June, 118(6): 2209-2218

Ghia JE, Blennerhassett P, Deng Y, Verdu E, Khan WI and Collins SM. Re-activation of inflammatory bowel disease in a mouse model of depression. Gastroenterology 2009; June, 136(7): 2280-2288

Ghia JE, Li N, Wang H, Collins M, Deng Y, El-Sharkawy RT, Cote F, Mallet J and Khan WI. Serotonin has a key role in pathogenesis of experimental colitis. Gastroenterology 2009; Nov, 137(5): 1649-1660

Khan WI and Ghia JE. Gut hormones: Emerging Role in Immune Activation and Inflammation. Clin. Exp. Immunol. 2010; Jul, 161(1): 19-27

Hasnain SZ, Wang H, Ghia JE, Haq N, Deng Y, Grencis RK, Velcich A, Thornton DJ and Khan WI. Mucin Gene Deficiency in Mice Impairs Host Resistance to Enteric Parasitic Infection. Gastroenterology 2010; May, 138(5): 1763-1771

Ghia JE, Blennerhassett P, Khan WI, Collins SM. The adoptive transfer of susceptibility to colitis by macrophages from mice with depression-like behavior. Inflammatory Bowel Disease 2011; Jul, 17(7): 1474-1489

Ghia JE, Li N, Wang H, Cote F, Suehiro Y, Mallet J & Khan WI. Serotonin activates dendritic cell function in the context of gut inflammation. Am. J. Pathol. 2011; Feb, 178(2): 662-671.  (Equal contribution)

Rahimian R, Dehpour AR, Fakhfouri G, Khorramizadeh MR, Ghia JE, Seyedabadi M, Caldarelli A, Mousavizadeh K, Forouzandeh M, Mehr SE. Tropisetron upregulates cannabinoid CB1 receptors in cerebellar granule cells: possible involvement of calcineurin. Brain Res. 2011; Oct, 1417: 1-8.

Fakhfouri G, Rahimian R, Ghia JE, Khan WI, Dehpour AR. Impact of 5HT3 receptor antagonists on peripheral and central disease. Drug Discov. Today 2012 Jul;17(13-14):741-7

Thanasupawat T, Hammje K, Adham I, Ghia JE, Del Bigio MR, Krcek J, Hoang-Vu C, Klonisch T, Hombach-Klonisch S. INSL5 is a novel marker for human enteroendocrine cells of the large intestine and neuroendocrine tumours. Oncol. Rep. 2013, Jan, 29(1):149-54

Kim JJ, Bridle BW, Ghia JE, Wang H, Manocha MM, Rengasamy P, Shajib MS, Wan Y, Hedlund PB, Khan WI. Targeted inhibition of serotonin type 7 (5-HT7) receptor function modulates immune responses and reduces the severity of intestinal inflammation. J. Immunol. 2013, May, 190(9): 4795-804

Park AJ, Collins J, Blennerhassett PA, Ghia JE, Verdu EF, Bercik P, Collins SM. Altered colonic function and microbiota profile in a mouse model of chronic depression. Neurogastrol. Motil. 2013, Sept, 25(9): 733-e575

Shajib MS, Wang H, Kim JJ, Sunjic I, Ghia JE, Denou E, Collins M, Denburg JA, Khan WI. Interleukin 13 and serotonin: linking the immune and endocrine systems in intestinal inflammation, PLOS ONE, 2013, Aug, 28;8(8), e72774

Khafipour E & Ghia JE. Mode of delivery and inflammatory disorders. Journal of Immunology & Clinical Research, September 2013. In press

Rahimian R; Fakhfouri G; Samadi P; Mehr SE; Ghia JE; Genazzani AA; Dehpour AR; Mousavizadeh K; Lim D. Tropisetron Attenuates Amyloid-Beta-Induced Inflammatory and Apoptotic Responses and cognitive disturbance in Rats. Eur. J. Clin. Invest. 2013, Oct, 43(10): 1039-1051

Gharedaghi MH, Seadabadi M, Ghia JE, Rahimian R. The role of different serotonin receptor subtypes in seizure susceptibility. Exp. Brain. Res. 2014, Feb, 232 (2): 347-367

Ji H, Rabbi MF, Labis B, Pavlov VA, Tracey KJ, Ghia JE. Central cholinergic activation of a vagus nerve - to spleen circuit alleviates experimental colitis. Mucosal Immunol. 2014, Mar, 7(2): 335-347 (Equal contribution)

Nagy JI, Urena-Ramirez V, Ghia JE. Functional deviations in gut contractility after connexin36 ablation and evidence for gap junctions forming electrical synapses between nitrergic enteric neurons. FEBS Letters, 2014, Apr, 588 (8): 1480-1490

Rabbi MF; Labis B; Metz-Boutigue MH; Bernstein CN; Ghia JE. Catestatin decreases macrophage function in two mouse models of experimental colitis. Biochem. Pharmacol. 2014, Jun, 89 (3): 386-398

Munyaka P & Ghia JE. Early childhood establishment of gut microbiota and subsequent health implications. Frontier in Pediatrics, September 2014, In press

Munyaka P, Rabbi MF, Pavlov VA, Tracey KJ, Khafipour E, Ghia JE. Central muscarinic cholinergic activation alters dendritic cells function in experimental colitis. PLOS ONE, 2014, Sept, DOI: 10.1371/journal.pone.0109272