Campylobacter jejuni
is a leading cause of bacterial-derived gastroenteritis worldwide.Campylobacteris most commonly acquired through the consumption of undercooked poultry meat or through drinking contaminated water. Following ingestion,Campylobacteradheres to the intestinal epithelium and mucus layer, causing toxin-mediated inflammation and inhibition of fluid reabsorption. Currently, the human response to infection is relatively unknown and animal hosts that model those responses are rare. As such, we examined patient fecal samples for the accumulation of the neutrophil protein, calgranulin C, during infection withCampylobacter jejuni.In response to infection, calgranulin C was significantly increased in the feces of humans. To determine whether calgranulin C accumulation occurs in an animal model, we examined for disease in ferrets. Ferrets were effectively infected byC. jejuniwith peak fecal loads observed at day three post-infection and full resolution by day 12. Serum levels of IL-10 and TNFa significantly increased in response to infection, which resulted in leukocyte trafficking to the colon. As a result, calgranulin C increased in the feces of ferrets at the time whenC. jejuniloads decreased. Further, the addition of purified calgranulin C toC. jejunicultures was found to inhibit growth in a zinc-dependent manner. These results suggest that upon infection withC. jejuni, leukocytes trafficked to the intestine release calgranulin C as a mechanism for inhibitingC. jejunigrowth.