Heme Acquisition in Campylobacter jejuni using the Chu Heme Transport System and its Role in Colonization and Pathogenesis.

This paper investigates the Campylobacter jejuni Chu heme transport system and its impact on pathogenesis. Campylobacter jejuni is one of the most common causes of bacterial gastroenteritis. The ability of C. jejuni to take up iron is an important factor in survival, particularly under low-iron conditions. For this purpose, the chu operon encoding chuA, chuB, chuC, and chuD was investigated by generating specific knockout mutants. Growth experiments tested these mutant strains’ capabilities in vitro under iron-restricted conditions with heme supplementation. Furthermore, the C57BL6 IL-10^-/- knockout mice were employed to assess the role of these genes in vivo. The ChuA heme receptor was identified as essential for growth under iron-limited conditions, while other genes in the operon demonstrated compensatory mechanisms. In vivo, all chu knockout strains exhibited significantly reduced fitness compared to wild-type C. jejuni, indicating that disrupted heme uptake adversely affects microbial survival. Furthermore, organ-specific differences in chu gene expression suggest that host factors, including diet, microbiome composition, and immune interactions, play critical roles in the fitness of chu knockout mutant strains.