Diarrheal diseases are a significant cause of global morbidity and mortality with a projected 4.48 billion annual cases and 1.66 million deaths. Many of these cases are due to gastrointestinal infection by a variety of bacterial, eukaryotic, and viral pathogens. One of the leading causes of these infections are bacteria from the genus Campylobacter, which cause an estimated 172 million infections every year and 75,000 fatalities.

In the developing world, Campylobacter species are endemic, the sources of infection are poorly understood, and disease tends to be less inflammatory. Most notably, infection in these areas is more persistent, especially in pediatric patients, where it can lead to the development of enteric dysfunction and stunting. These observations have raised several questions, including i) are the differences between disease in developed and developing regions due to strain diversity, ii) are these differential outcomes due to host divergence, or iii) are they due to other factors like diet.these bacteria are thought to be acquired from contaminated water and cause brief bouts of mild diarrhea in adults, but can persistently colonize pediatric patients and lead to the development of a gastrointestinal disorder called environmental enteric dysfunction (EED). EED subsequently results in a reduced ability to acquire nutrients from food, which leads to decreased growth and cognitive development of these pediatric patients.

In the developed world, Campylobacter species often infect patients after consuming undercooked meat, including beef and poultry, where it can colonize the lower gastrointestinal tract and cause severe intestinal inflammation and diarrhea. While these infections are believed to often resolve without incident, recent studies have provided evidence that a variety of autoimmune and inflammatory disorders can occur following infection with Campylobacter. Importantly, despite these impacts, it remains unknown i) what host components are recruited to the site of infection and how might they have collateral effects on gastrointestinal tissue, ii) what unique bacterial components C. jejuni possesses that lead to this extraordinary immune response, and iii) how this response can become dysregulated and lead to the development of post-infectious disorders.

In addition to the above concerns, drug-resistant Campylobacter is becoming more prevalent and is listed as an ‘urgent threat’ to public health by both the CDC and WHO.

Because of the above gaps in knowledge and the lack of novel strategies to reduce disease, our group is active in three areas:

1. Understanding the host response to C. jejuni infection and how certain components of the inflammatory response are responsible for gastrointestinal and extraintestinal diseases.

2. Identifying and characterizing the C. jejuni factors that contribute to infection and immune activation of susceptible hosts.

3. Leveraging what we learn to develop strategies that reduce C. jejuni infection or disease severity.