Role of eptC in Biofilm Formation by Campylobacter jejuni NCTC11168 on Polystyrene and Glass Surfaces.

The complex roles of cell surface modification in the biofilm formation of , a major cause of worldwide foodborne diarrheal disease, are poorly understood. In a screen of mutants from random transposon mutagenesis, an insertional mutation in the eptC gene (cj0256) resulted in a significant decrease in NCTC11168 biofilm formation (<20%) on major food contact surfaces, such as polystyrene and borosilicate glass, when compared with wild-type cells (p < 0.05). In strain 81-176, the protein encoded by modified cell surface structures, such as lipid A, the inner core of lipooligosaccharide, and the flagellar rod protein (FlgG), by attaching phosphoethanolamine. To assess the role of in NCTC11168, adherence and motility tests were performed. In adhesion assays with glass surfaces, the mutant exhibited a 0.77 log CFU/cm² decrease in adherence compared with wild-type cells during the initial 2 h of the assay ( < 0.05). These results support the hypothesis that the modification of cell surface structures by affects the initial adherence in biofilm formation of NCTC11168. In motility tests, the mutant demonstrated reduced motility when compared with wild-type cells, but wild-type cells with the transposon inserted in a gene irrelevant to biofilm formation (cj1111c) also exhibited decreased motility to a similar extent as the mutant. This suggests that although affects motility, it does not significantly affect biofilm formation. This study demonstrates that is essential for initial adherence, and plays a significant role in the biofilm formation of NCTC11168.