Haemophilus influenzae (Hi) is a host-adapted human pathogen that can cause both invasive and non-invasive disease. It can persist in different human body niches that vary in carbon metabolite and oxygen availability. It has been shown in other pathogens such as Salmonella enterica that central metabolism enzymes contribute significantly to survival in the host, and similar mechanisms might be playing a role in Hi pathogenicity. Previous work in our laboratory demonstrated that two Hi strains employed different pathways to degrade glucose, indicating that a repertoire of diverse metabolic states can support Hi survival and likely determine outcomes of host-bacteria interactions (Othman et al., 2014).
In this study, we have investigated specific metabolic patterns in two Hi strains, NTHi R2866 (R2866) and NTHi C188 (C188), both of which cause invasive disease. We expected that if Hi metabolism is specific for a particular body niche, then both strains should show similar metabolic profiles that should be different from the ones described previously. In this work, we showed that R2866 and C188 have identical gene profiles for central metabolic and respiratory pathways. However, there were significant differences in the basic properties of strains. R2866 showed significantly increased growth under microaerophilic condition, and much stronger self-aggregation properties than C188. Biofilm formation did not vary with oxygen tension in either strains, but again R2866 always produced a very large amount of biofilm while C188 did not. In contrast to this, NMR-derived metabolomics profiles of the two strains were similar with formate and acetate being key metabolites during aerobic and microaerophilic growth, respectively. High expression of genes involved in lactate metabolism and pyruvate conversions were observed, while observed changes in gene expression were mostly associated with the respiratory chain genes.