Abstract
The interaction of bacterial pathogens with mammalian hosts leads to a variety of physiological responses of the interacting partners aimed at an adaptation to the new situation. These responses include multiple metabolic changes in the affected host cells which are most obvious when the pathogen replicates within host cells as in case of intracellular bacterial pathogens. While the pathogen tries to deprive nutrients from the host cell, the host cell in return takes various metabolic countermeasures against the nutrient theft. During this conflicting interaction, the pathogen triggers metabolic host cell responses by means of common cell envelope components and specific virulence-associated factors. These host reactions generally promote replication of the pathogen. There is growing evidence that pathogen-specific factors may interfere in different ways with the complex regulatory network that controls the carbon and nitrogen metabolism of mammalian cells. The host cell defense answers include general metabolic reactions, like the generation of oxygen- and/or nitrogen-reactive species, and more specific measures aimed to prevent access to essential nutrients for the respective pathogen. Accurate results on metabolic host cell responses are often hampered by the use of cancer cell lines that already exhibit various de-regulated reactions in the primary carbon metabolism. Hence, there is an urgent need for cellular models that more closely reflect the in vivo infection conditions. The exact knowledge of the metabolic host cell responses may provide new interesting concepts for antibacterial therapies.
Highlights
Interactions between eukaryotic organisms and prokaryotes are ubiquitous
For a better understanding of the complex problem, we present in the first part of this review a condensed overview on the major metabolic pathways, nutrient transporters, receptors and regulators controlling the metabolism in mammalian cells, as these metabolic cell processes are potential host cell targets for the interaction with components of the bacterial pathogens
The studies with L. monocytogenes-infected “humanized” mice and with primary mouse macrophages show that L. monocytogenes induces reactions of the host cell carbon metabolism that favor uptake of glucose and the production of compounds, such as glucose-6P, serine, and glycerol, which are preferably utilized by the bacteria for their own intracellular metabolism (Eylert et al, 2008)
Summary
Interactions between eukaryotic organisms and prokaryotes are ubiquitous. These encounters may affect the metabolism of the interacting partners in different ways, resulting in beneficial, neutral, or detrimental outcome for the partners. As shown by numerous transcriptome studies (carried out in established mammalian cell lines, primary phagocytes, or different animal infection models), many of these metabolic responses are unspecific, i.e., they occur with most extracellular and intracellular bacterial pathogens and even with non-pathogenic or killed bacteria and are termed “core host responses” (Boldrick et al, 2002).
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