Abstract
Campylobacter jejuni is the leading food-borne poisoning in industrialized countries. While the bacteria causes disease in humans, it merely colonizes the gut in poultry or pigs, where seems to establish a commensal relationship. Until now, few studies have been conducted to elucidate the relationship between C. jejuni and its different hosts. In this work, a comparative proteomics approach was used to identify the underlying mechanisms involved in the divergent outcome following C. jejuni infection in human and porcine host. Human (INT-407) and porcine (IPEC-1) intestinal cell lines were infected by C. jejuni for 3 h (T3h) and 24 h (T24h). C. jejuni infection prompted an intense inflammatory response at T3h in human intestinal cells, mainly characterized by expression of proteins involved in cell spreading, cell migration and promotion of reactive oxygen species (ROS). Proteomic analysis evidenced significantly regulated biofunctions in human cells related with engulfment and endocytosis, and supported by canonical pathways associated to infection such as caveolar- and clathrin-mediated endocytosis signaling. In porcine IPEC-1 cells, inflammatory response as well as signaling pathways that control cellular functions such as cell migration, endocytosis and cell cycle progression resulted downregulated. These differences in the host response to infection were supported by the different pattern of adhesion and invasion proteins expressed by C. jejuni in human and porcine cells. No marked differences in expression of virulence factors involved in adaptive response and iron acquisition functions were observed. Therefore, the results of this study suggest that both host and pathogen factors are responsible for commensal or infectious character of C. jejuni in different hosts.
Highlights
Human campylobacteriosis is leading the rank of food-borne diseases in developed countries, with Campylobacter being the most regularly reported zoonotic pathogen in the European Union since 2005 (EFSA, 2015)
The results of this analysis (Table S2) predicted a significant activation of the inflammatory response, increased at T3h compared to T24h, and associated to the differential expression of many proteins involved in cell migration and infiltration, cell movement, cytoskeleton organization and promotion of reactive oxygen species (ROS)
Ingenuity Pathway Analysis (IPA) analysis predicted that infection of cells, molecular transport and synthesis of proteins were functions activated at T3h and reduced at T24h
Summary
Human campylobacteriosis is leading the rank of food-borne diseases in developed countries, with Campylobacter being the most regularly reported zoonotic pathogen in the European Union since 2005 (EFSA, 2015). This study showed that a strong inflammatory response occurred in human cells after bacterial infection while no response was observed in intestinal epithelial cells of porcine origin. Despite these results, much is still unknown about why Campylobacter is pathogenic to humans and not to other species such as pigs. We surveyed the proteome of human and porcine intestinal epithelial cells after C. jejuni infection in order to elucidate the molecular mechanisms underlying the pathological or commensal behavior of Campylobacter in different hosts
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