The gastrointestinal pathogen Campylobacter jejuni metabolizes sugars with potential help from commensal Bacteroides vulgatus.

Although the gastrointestinal pathogen Campylobacter jejuni was considered asaccharolytic, >50% of sequenced isolates possess an operon for L-fucose utilization. In C. jejuni NCTC11168, this pathway confers L-fucose chemotaxis and competitive colonization advantages in the piglet diarrhea model, but the catabolic steps remain unknown. Here we solved the putative dehydrogenase structure, resembling FabG of Burkholderia multivorans. The C. jejuni enzyme, FucX, reduces L-fucose and D-arabinose in vitro and both sugars are catabolized by fuc-operon encoded enzymes. This enzyme alone confers chemotaxis to both sugars in a non-carbohydrate-utilizing C. jejuni strain. Although C. jejuni lacks fucosidases, the organism exhibits enhanced growth in vitro when co-cultured with Bacteroides vulgatus, suggesting scavenging may occur. Yet, when excess amino acids are available, C. jejuni prefers them to carbohydrates, indicating a metabolic hierarchy exists. Overall this study increases understanding of nutrient metabolism by this pathogen, and identifies interactions with other gut microbes.

Role of glucocorticoids and Toxoplasma gondii infection on murine intestinal epithelial cells.

Glucocorticoids (GCs) are stress hormones secreted in response to perceived psychological and or physiological stress. GCs have been shown to reduce tissue inflammation by down-regulating the production of inflammatory chemokines produced by epithelial cells. The protozoan parasite Toxoplasma gondii is known to increase cytokine, chemokine, and Toll-like receptors (TLRs) expression in parasite infected mouse intestinal epithelial cells (IECs). We sought to analyze the role of an anti-inflammatory protein, glucocorticoid-induced leucine zipper (GILZ) in MODE-K cells during infection with T. gondii. GILZ expression in MODE-K cells was assessed by PCR and immunoblotting after stimulation with GCs (corticosterone, CORT) or T. gondii infection. GILZ mRNA was constitutively expressed in MODE-K cells but not its protein product. While infection and pre-exposure to CORT decreased GILZ isoforms of 28 and 17 kD, the presence of CORT during infection increased levels of 17 kD isoform. Infected cells treated with CORT had decreased expression of chemokines (IP-10/CXCL10, MCP-1/CCL2, MIP-2/CXCL8) while their expression was increased when endogenous GILZ was removed by siRNA treatment. GILZ up-regulation during infection may serve as a mechanism to decrease epithelial cell responses and facilitate parasite replication.