![]() coli, including increased transcription of gene clusters involved in siderophore biosynthesis. Under iron-limiting conditions, an increase in L-ornithine levels induces a transcriptional response in E. The end product of this pathway, L-ornithine, is secreted into the environment. faecalis utilizes the arginine deiminase pathway to generate energy from arginine. coli to enhance production of siderophores under iron-starvation conditions ( Keogh et al., 2016).īased on these findings, the following scenario could unfold ( Figure 1): during wound infection, E. faecalis secretes a simple metabolite, L-ornithine, which acts as a cue for E. Through the elegant combination of unbiased omics approaches, including RNA-seq, metabolomics, and classical transposon mutagenesis, the authors found that E. The synergy observed in vivo was recapitulated in vitro when the two bacteria were co-cultured under iron limiting conditions, giving the authors an opportunity to mechanistically dissect this phenomenon. This finding is consistent with previous reports ( Montravers et al., 1994 Lavigne et al., 2008). coli growth in a mouse model of wound infection, suggesting a synergistic polymicrobial interaction. coli using in vitro co-culture models and a murine model of wound infection. (2016) investigate potential synergistic interactions between E. In this issue of Cell Host & Microbe, Keogh et al. While the battle for iron in monobacterial infections has been well described, its role in polybacterial infections remains poorly understood.Įnterococcus faecalis and Escherichia coli are frequent causes of catheter-associated urinary tract infections, surgical site infections, and wound infections, either as monomicrobial or polymicrobial infections. ![]() For example, bacteria use alternative metals in metalloenzymes, utilize heme uptake systems, directly acquire iron from transferrin and lactoferrin, efficiently import any free iron ions, and produce iron-chelating siderophores. Conversely, bacterial pathogens have evolved to use a number of different strategies to overcome iron starvation inside the host. To limit bacterial access to iron, the host stores iron intracellularly, and extracellular iron is bound by the host proteins transferrin or lactoferrin. ![]() Not surprisingly, the control of iron is a key battle between host and pathogen during bacterial infection. ![]() As an excellent redox catalyst in many fundamental cellular processes, including respiration and DNA replication, iron is essential for both humans and bacteria. However, the mechanisms shaping the complex interplay between the host and its multiple microbial populations are poorly understood.ĭuring infection, an important and well-studied strategy of host defense is iron limitation (reviewed in Cassat and Skaar, 2013). While polymicrobial interactions can affect the host, the host can also impact the environment in which these interactions occur. The phenomenon is termed polymicrobial synergy and defined as “an interaction of two or more microbes in an infection site that results in enhanced disease compared to infections containing the individual microbe acting alone” (reviewed in Murray et al., 2014). Polymicrobial infections play important roles in gastrointestinal, urinary tract, wound, and lung infections, and their impacts can be more detrimental to the host than infections involving the individual microbes alone. ![]()
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