Almost all bacteria require iron for their survival. For many bacterial pathogens, the ability to utilize heme as an iron source is essential for their survival and virulence. The opportunistic pathogen Pseudomonas aeruginosa encodes two heme uptake systems, the Pseudomonas heme uptake (phu) and heme assimilation systems (has). Consistent with recent clinical studies, we have shown the Has and Phu systems have non-redundant roles in heme sensing and transport, respectively. Combining 13C-heme isotopic labeling and bacterial genetics together with biophysical studies we have further shown the cytoplasmic heme chaperone PhuS is critical in linking heme flux through HemO to post-transcriptional regulation of the Has system by the heme metabolite biliverdin IXΒ (BVIXβ). Additionally, we present evidence that BVIXβ has functions as a signaling molecule in the complex regulation of virulence associated systems such as siderophore/metallophore biosynthesis (pyochelin and pseudopaline), quorum sensing (phenazine biosynthesis), motility and biofilm formation. Coupling the heme sensing and utilization to the regulation of critical virulence factors, provides a mechanism for the cell to rapidly respond and adapt to changes within the host environment. Furthermore, BVIXβ represents an important secondary metabolite in the extensive signaling repertoire of Pseudomonas aeruginosa.

Seeing red: The role of heme in Pseudomonas aeruginosa virulence and pathogenesis

255th National Meeting (2018)

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