Efficient colonic colonization by Campylobacter jejuni requires the heme receptor ChuA

A recent study explored the role of the heme receptor ChuA in Campylobacter jejuni's ability to colonize the colon and cause disease. Previous research had shown that the bacterium possesses a heme utilization system that enables growth in iron-deprived environments, with transcription of this system being stimulated during human infections. However, the necessity of this heme transport system for colonization and associated pathology remained unclear.

To investigate this, researchers created deletion mutants of each component in the heme transport system and evaluated their capacity to facilitate heme-dependent growth and iron uptake. The findings revealed that only ChuA was essential for heme-dependent growth and iron acquisition, reinforcing earlier findings by another research group. Additionally, the impact of these mutants on intestinal colonization, immune activation, and pathology was examined.

The study observed that increased heme levels and expression of the chuABCD genes occurred during Campylobacter jejuni infection of IL-10-/- mice. When the heme receptor ChuA was mutated, there was a significant reduction in colonic colonization. Furthermore, neutrophil and circulating monocyte recruitment to the colon during infection were significantly diminished with the ChuA mutant, although populations of self-sustaining tissue macrophages remained unchanged.

The absence of ChuA led to decreased colonic colonization and was associated with reduced innate immune cell recruitment and intestinal pathology.

In summary, the research conclusively established that ChuA-dependent heme acquisition plays a crucial role in efficient colonic colonization and the subsequent inflammatory disease caused by Campylobacter jejuni.