ABSTRACTCampylobacter jejuniis a major cause of bacterial food-borne enteritis worldwide, and invasion into intestinal epithelial cells is an important virulence mechanism. Recently we reported the identification of hyperinvasiveC. jejunistrains and created a number of transposon mutants of one of these strains, some of which exhibited reduced invasion into INT-407 and Caco-2 cells. In one such mutant the transposon had inserted into a homologue ofcj1136, which encodes a putative galactosyltransferase according to the annotation of theC. jejuniNCTC11168 genome. In the current study, we investigated the role ofcj1136inC. jejunivirulence, lipooligosaccharide (LOS) biosynthesis, and host colonization by targeted mutagenesis and complementation of the mutation. Thecj1136mutant showed a significant reduction in invasion into human intestinal epithelial cells compared to the wild-type strain 01/51. Invasion levels were partially restored on complementing the mutation. The inactivation ofcj1136resulted in the production of truncated LOS, while biosynthesis of a full-length LOS molecule was restored in the complemented strain. Thecj1136mutant showed an increase in sensitivity to the bile salts sodium taurocholate and sodium deoxycholate and significantly increased sensitivity to polymyxin B compared to the parental strain. Importantly, the ability of the mutant to colonize 1-day-old chicks was also significantly impaired. This study confirms that a putative galactosyltransferase encoded bycj1136is involved in LOS biosynthesis and is important forC. jejunivirulence, as disruption of this gene and the resultant truncation of LOS affect both colonizationin vivoand invasivenessin vitro.
A σ28-Regulated Nonflagella Gene Contributes to Virulence of Campylobacter jejuni 81-176