Bacteria reprogram our cellular metabolism- why?
by Sam Gild
Metabolism is important- by definition, it maintains life. We know that nothing in nature is ‘random’- everything evolves by natural selection, which necessitates selective pressure. Metabolism has evolved to fit the needs of the organism it serves, and it is accordingly very diverse. By way of example, mycobacterium tuberculosis (Mtb) utilizes an enormously flexible metabolism, allowing it to thrive in diverse niches in its human host, each with its own nutrient and biochemical composition.
Mtb is but one of many intracellular infectious bacteria that has been shown to alter the metabolism of the cell that it infects. Though we know that this occurs, we have yet to unravel exactly how and, crucially, ‘why’. As we have discussed, a ‘why’, there must be. Escoll and Buchrieser (2018), sought to compile all the relevant evidence, by way of published scientific literature. This was in order to thematize and characterize our understanding of this phenomenon – the how, and ‘why’.
The conclusion of this review was that metabolic changes in the host cell were not incidental. The host cell is selectively re-programmed by the invading bacteria in order to meet the metabolic needs of the pathogen- this is the ‘why’. Just as Mtb reprograms its host-cell to produce more lipids (which are crucial to Mtb’s survival), yet other bacteria, such as Chlamydia, utilize host-derived energy-rich substrates that are not very important to the host cell but are hugely beneficial to the respective bacterium- so-called ‘bipartite metabolism’. We may thus think of the metabolism of many a bacterial species as including the co-opted metabolism of its host cell. In addition to a broader definition of metabolism and the ‘why’ of metabolic re-programming, this intriguing work shows us that we (our cellular metabolisms) are not as autonomous or inflexible as we once thought- we are a metabolically malleable organism that lives vicariously through interactions with our bio-environments.
Reference:
Escoll P, Buchrieser C. Metabolic reprogramming of host cells upon bacterial infection: Why shift to a Warburg-like metabolism?. FEBS J. 2018;285(12):2146-2160. doi:10.1111/febs.14446
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