FARE’s 2017 Research Retreat takes place this weekend, March 31-April 1, in Tysons Corner, VA. Among the presenters will be Dr. Simon Hogan (Cincinnati Children’s Hospital Medical Center), who received a FARE Investigator in Food Allergy Award in 2015. Dr. Hogan’s lab is investigating how proteins released at the start of an allergic response can cause blood vessels to leak during life-threatening anaphylaxis. Understanding the chain of chemical events that leads to anaphylactic shock is a key step in devising strategies to prevent severe food allergy symptoms. Dr. Hogan explained his work late last year in FARE’s Research Advocate newsletter.
What first attracted you to food allergy research?
I have had an interest in allergic inflammation since my days as a PhD student working alongside Professor Paul Foster in Australia over 20 years ago. Following my PhD, I came to Cincinnati Children’s to work alongside Professors Marc Rothenberg and Fred Finkelman, and this is where my intrigue for gastrointestinal allergic inflammatory responses, such as those seen in eosinophil-associated gastrointestinal diseases and anaphylaxis, developed. Since those early days, I have become increasingly interested in understanding the “how,” “when” and “why” of food allergy. It actually keeps me up at night!
What has sustained your interest?
(1) Attending Cincinnati Children’s Allergy and Immunology case report presentations. Time after time, our outstanding allergists and fellows speak of the constant stress that food allergy causes both the children and the families.
(2) The frustration of our allergists in their inability to adequately deal with food allergy. When food avoidance is the mainstay therapeutic approach to prevent a reaction, we need to do better. To me, this relates to our lack of understanding of the immunologic processes involved in food allergy, and that is where I think I can contribute.
What experimental finding has surprised you the most, and why?
One of the main instigators of food allergy is an immune cell called a CD4+, Th2 cytokine-producing, “pro-allergic” cell. This cell communicates with other immune cells and sets the stage for an acute food allergic reaction. One thing that has surprised me is that despite all the research, we are unable to switch a CD4+, Th2 cytokine-producing, “pro-allergic” cell into a “non-allergic” cell. We can prevent the cell from becoming pro-allergic, and we can temporally suppress the pro-allergic cell. However, for reasons that we do not know but are continuing to investigate, we cannot switch the “proallergic” cell to a non-allergic cell to stop the underlying allergic response in its tracks.
How might your research that is supported by a FARE Investigator in Food Allergy Award affect patient care in the future?
My group and I have a keen interest in understanding what immunologic processes alter the severity of a food-induced anaphylactic reaction. The FARE Investigator in Food Allergy Award has helped support the significant progress we’ve made in understanding what immune steps worsen food anaphylactic reactions and, at least in an experimental context, in putting the brakes on these reactions by inhibiting a certain pathway. From our current data and hypotheses, we predict that blockade of this pathway may not prevent a reaction but will probably reduce the likelihood of the reaction being severe and life-threatening. We think that this may be very useful for people with known food allergies and for individuals who are undergoing immune therapy approaches, as inhibiting this pathway would reduce the likelihood of a reaction and the degree of its severity.
What unresolved question relating to food allergies would you most like to see answered?
I have a lot of questions. However, the main two questions are:
(1) How do we switch the CD4+, Th2 cytokine-producing, “pro-allergic” cell into a “non-allergic” cell?
(2) Can we prevent severe food reactions from occurring? Hopefully, my PhD student Amna Yamani will have an answer to this second question sometime soon!