McMaster University

McMaster University

Manel Jordana

, MD, PhD

Pathology and Molecular Medicine

Division: Molecular Medicine
McMaster Immunology Research Centre

McMaster University
4013 Michael DeGroote Centre for Learning & Discovery
905-525-9140 ext. 22374

Currently accepting Graduate Students
Currently accepting Post-Doctoral Fellows

Manel Jordana

Faculty Biography

Education and Professional Standing

  • PhD, McMaster University, 1989
  • MD, Universitat Autonoma (Spain), 1976


Research Focus

Our laboratory is focused on understanding the origin and evolution of allergy and allergic diseases. Our research activities are grouped into two main directions: allergic airway disease, particularly asthma, and food allergy, particularly peanut allergy. At present, it is estimated that approximately 40% of individuals in developed countries are allergic, or have atopy. However, this does not mean that they all suffer from allergic diseases. Indeed, the current prevalence of allergic asthma is ≈10%, almost 2/3 of those affected are children under 18 years of age. In addition, the prevalence of food allergy is ≈3.5%, and that of peanut allergy ≈1.5%; importantly, peanut allergy is the major culprit of anaphylaxis, a life threatening condition. Overall, the prevalence of allergic diseases has dramatically increased over the last several decades.

The major thrust of our laboratory is directed at studying the immunobiology of allergic asthma and peanut allergy/anaphylaxis in in vivo experimental systems. In reference to our research on allergic asthma, our major interest is in understanding the origin and evolution of allergic airway disease; specifically:

  • Investigating the impact of environmental and host variables on the susceptibility to develop and exacerbate allergic airway disease
  • Decoding the precise relationship that may exist among allergic sensitization, airway inflammation, airway remodelling and lung function.

Historically, a unique tenet of our approach has been the modification of the airway environment by means of gene transfer technology, i.e. the introduction of genes that will express molecules for an extended, albeit transient, period of time. Using these approaches, we established novel models of mucosal sensitization and investigated how certain molecules can facilitate, amplify, deviate or prevent allergic responses. In a further effort to recapitulate human disease, our laboratory was among the first to establish models using common aeroallergens, particularly house dust mite (the most pervasive common indoor allergen worldwide) and ragweed (a typical and common outdoor allergen).The recognition of asthma as a complex disease has important implications. First, complex and dynamic systems are very sensitive to perturbations in the initial conditions. Thus, we are engaged in projects investigating the impact of specific molecules and viruses (e.g. influenza A) on the thresholds of allergen required to trigger allergic responses. Second, the need for precise quantification has led us to develop new modeling strategies, in vivo as well as in silico, that incorporate mathematical approaches in collaboration with scientists in the Department of Mathematics.

In reference to our research on peanut allergy/ anaphylaxis, our major interests evolve along two main directions:

  • Understanding the mechanisms underlying sensitization to peanut, i.e. how and why some individuals become allergic.
  • Investigating the role of effector molecules in anaphylaxis with a view to develop strategies that can reduce the severity and, hopefully, control/prevent anaphylactic reactions.

Food allergy is thought to develop due to a lack of induction, or disruption in, oral tolerance. The “Hygiene Hypothesis” purports that early microbial exposure decreases the risk of developing allergies or, alternatively, increases the likelihood of tolerance induction. In line with this hypothesis is the notion that the extensive life-long communication between the immune system and more than 1014 resident gut bacteria critically influences whether tolerance or allergic disease develops upon antigen ingestion. Thus, we think that the finely timed evolution of resident gut flora impacts early host immune programming and, thus, likely influences the immunological response, oral tolerance versus sensitization, which ensues upon an initial encounter with antigen. Consequently, improper or inadequate maturation of the immune system may result in aberrant responses to ingested antigens and ultimately, food allergy. We have established several mouse models of peanut allergy and anaphylaxis, and an ongoing extension of this work involves the use of axenic and gnotobiotic animals in collaboration with scientists in the Farncombe Family Digestive Health Research Institute. In addition, clinical research in this area is conducted in collaboration with Dr. Susan Waserman. The goals of this research are: to develop better tools to determine who is truly allergic to peanut and, b) to implement immunotherapy strategies.

Academic Interests

Dr. Jordana currently teaches Inquiry I (HTH SCI 3E06) for the Bachelor of Health Sciences Program, acting as a facilitator for first year students. He also teaches within the Molecular Immunology, Virology and Inflammation Faculty for the Health Sciences Graduate Program.


Selected Publications

Visit Dr Jordana's McMaster Immunology Research Centre (MIRC) web profile for more informatlion


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