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  1. Cong T. Trinh - Google Scholar Citations
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  3. Metabolic reprogramming by viruses in the sunlit and dark ocean

Applied microbiology and biotechnology 81 5 , , Applied microbiology and biotechnology 95 4 , , Biotechnology and bioengineering 11 , , Journal of Computational Biology 17 2 , , Applied microbiology and biotechnology 99 10 , , Biotechnology and bioengineering 8 , , Metabolic engineering communications 3, , Articles 1—20 Show more. Help Privacy Terms. Elementary mode analysis: a useful metabolic pathway analysis tool for characterizing cellular metabolism CT Trinh, A Wlaschin, F Srienc Applied microbiology and biotechnology 81 5 , , Design, construction and performance of the most efficient biomass producing E.

The fractional contributions of elementary modes to the metabolism of Escherichia coli and their estimation from reaction entropies AP Wlaschin, CT Trinh, R Carlson, F Srienc Metabolic engineering 8 4 , , Rational design and construction of an efficient E. Elucidating and reprogramming Escherichia coli metabolisms for obligate anaerobic n-butanol and isobutanol production CT Trinh Applied microbiology and biotechnology 95 4 , , Enhancing fatty acid ethyl ester production in Saccharomyces cerevisiae through metabolic engineering and medium optimization RA Thompson, CT Trinh Biotechnology and bioengineering 11 , , Expanding the modular ester fermentative pathways for combinatorial biosynthesis of esters from volatile organic acids DS Layton, CT Trinh Biotechnology and bioengineering 8 , , THP-1 is a human monocytic leukemic cell line which—although defective in p53 Sugimoto et al.

This study, albeit performed with a cell line, nevertheless provides some interesting conclusions concerning metabolic reprogramming of host cells in support of Mt replication: i The original metabolic program of un-infected THP-1 cells apparently provides suitable conditions for the initial intracellular replication of Mt; this program is clearly different from the TLRmediated metabolic program described above. This is probably linked to the increased glucose uptake which is again observed by the virulent mycobacterial strains only.

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Finally, similar to Salmonella , up-regulation rather than down-regulation of p53 seems to occur in Mt - infected MPs which may be important for suppression of apoptosis Galietti et al. The pathogen apparently exploits this change in host metabolism to support its own growth and survival Czyz et al. Whether there is a link between this interaction and the observed shift to a Warburg-like metabolism in the Brucella -infected THP-1 cells is difficult to decide as in both studies cell lines of different origin are used as host cells.

Thus, both observations suggest an essential role of aerobic glycolysis for providing glucose as essential nutrient for intracellular Brucella replication.


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This assumption is in line with a report showing that B. Glucose uptake by intracellular Brucellae appears to be crucial for their replication in AAMs, as inactivation of the bacterial GLUT, GluP, inhibits intracellular survival in these host cells Xavier et al. However, the canonical Atg5-dependent macroautophagic pathway is dispensable for replication of B. The obligate intracellular pathogen C. Little is known on metabolic reprogramming of these primary host cells by C.

However, using THP-1 cells it has been shown that sustained activation of Akt is required for intracellular replication of this pathogen and maintenance of host cell viability Voth and Heinzen, ; Hussain and Voth, Autophagy also seems to support intracellular replication of C. Substantial work has been carried out to analyze host cell responses upon infection by C.

Although most of these studies primarily concentrate on strategies that prevent host cell death upon infection, an important prerequisite for intracellular chlamydial proliferation Byrne and Ojcius, , some of these studies recognize the link between the anti-apoptotic effect and the generation of metabolic programs in the infected host cells that support efficient intracellular chlamydial replication.

Down-regulation of p53 in C.

Cong T. Trinh - Google Scholar Citations

Chlamydia -infected fallopian tube organoids show Myc activation which induces host cell HK-2, its translocation to the mitochondria and a Warburg-like effect Al-Zeer et al. Recently, a whole genome RNA interference screen combined with metabolic profiling identified numerous metabolic targets Rother et al. Elevated levels of pyruvate, lactate, and Glu indicated again a shift toward a Warburg-like metabolism. Pyruvate dehydrogenase kinase 2 PDK2 , a key enzyme regulating aerobic glycolysis, was identified as essential host factor for chlamydial replication and development Rother et al.

Intriguingly, these results were obtained in HeLa cells which already carry out a Warburg-like metabolism, indicating that aerobic glycolysis and a hypermetabolic state is supportive for Chlamydia replication. These conditions probably also favor the intracellular replication of B.

However, while in viral infections IFNs in general trigger antiviral responses see above , their role in the IBP infections appears to be more complex and enigmatic, i. On the other hand, also host-detrimental and pro-bacterial effects, especially by IFN-I, have been observed depending on the IBP, the host and the route of infection Perry et al. In summary, the activation of possible metabolic regulators, including several oncogenes e.

The link of these processes to immune responses, autophagy and cell death has been rather extensively analyzed.

These events are expected to also lead to metabolic reprogramming of the infected host cells which may support the intracellular IBP replication. However, up to now rather little information exists regarding this important aspect. IBPs are common bacterial partners in such co-infections. It is generally agreed that multifactorial processes involving interactions of yet poorly defined host, viral and bacterial factors are responsible for the emergence of these co-infections McCullers, , ; Jamieson et al.

However, little attention has been paid to the possibility that metabolic reprogramming in host cells triggered by the viral partner might support co-infection by the bacterial partner. While a is a generally accepted mechanism to explain co-infections Bell and Noursadeghi, , little experimental evidence exists for b and c. IAV predominantly infects respiratory epithelial cells. Streptococcus pneumoniae , a mainly extracellular pathogen Belon and Blanc-Potard, , is a frequently observed co-infecting partner.

The IAV infection causes release of free host sialic acid which serves as nutrient for the co-infecting S. In addition, IAV infection leads in these cells to an increase in c-Myc and associated with it to enhanced glycolysis and glutaminolysis Smallwood et al.

This reprogrammed cell metabolism most likely leads to enhanced production and release of lactate which is also a valuable energy and carbon source for S.

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The reprogramming of a low-active OXPHOS metabolic state into an aerobic glycolytic state with high glucose consumption and lactate production is a frequent event that occurs in primary host cells upon viral especially oncoviral infection Noch and Khalili, ; Mushtaq et al. This metabolic state is similar to the highly active metabolism observed in many established often virus-transformed cell lines which as pointed out above are in general excellent host cells for most IBPs.

Furthermore, lactate may serve as an efficient energy source for some IBPs when taken up and converted to pyruvate see above. It is therefore not unlikely that in vivo viral infections prepare a lusciously filled dining table for special bacterial guests which reach the virus-infected cells. So far there are, however, only hints and less hard facts supporting this hypothesis Seganti et al. Intracellular pathogens in general must reprogram the metabolism of their host cells to proliferate or persist in these infection niches. This is achieved by viruses mainly by the interaction of diverse, in part well-defined viral factors with specific metabolic control elements of the host cell, especially oncoproteins oncogenes and tumor suppressors, or by the introduction of viral oncogenes into the host cell as in case of oncogenic viruses.

The metabolic reprogramming often leads in the infected host cells to enhanced glucose uptake, aerobic glycolysis, production and secretion of lactate together with reduced activity of the TCA and OXPHOS i. In some cases, Gln may serve as additional or predominant carbon substrate which replenishes the TCA through glutaminolysis. The induced catabolism allows activation of anabolic pathways necessary for the production of the viral nucleic acids, capsids, and eventually membrane envelopes. Compared to the already advanced knowledge concerning the metabolic reprogramming of virus-infected cells, the corresponding cellular processes that are triggered by IBPs to allow their efficient replication are still poorly understood.

The reasons for this problem are diverse: In contrast to viruses, IBPs carry out an own metabolism that is in a pathogen-specific manner adapted to that of the host cell. The two metabolic fluxes are difficult to separate and to measure simultaneously.


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Only recently, methods have been developed to monitor IBP and host metabolism in parallel. The most sensitive method is dual RNA sequencing Westermann et al. However, metabolic fluxes are determined by the respective enzyme activities that are controlled in particular by post-transcriptional and post-translational processes. This means that even precise transcript data are of limited value for the determination of the actual metabolism of the two partners.

Metabolomics Nicholson and Lindon, ; Misra et al. For example, the MS or NMR analysis of the 13 C-profiles in bacteria-specific biosynthetic products such as mDAP and host -essential amino acids provides unequivocal information about the metabolic fluxes in the bacteria. On the other hand, this method in its present form is not very sensitive i. This means that the presently available methods only give us a rather rough idea about the metabolic reprogramming of the host cell during IBP infections and about the adapted intracellular metabolism of the IBP.

The second problem concerns the used host cells. Especially for infections caused by IBPs it is often even unclear what the primary host cell and its metabolic state is. Established cell lines, often used as host cell models for IBP and virus infections, have significant drawbacks for investigating metabolic issues related to infections, in particular when analyzing the metabolic reprogramming triggered by the pathogen.

The third and probably biggest problem is the investigation of the metabolism of infected host cells under the changing environmental in vivo conditions certainly different from the rich media conditions which are normally applied in in vitro studies. Only few of the studies discussed in this review addressed this problem. These drawbacks already indicate the necessary future developments: Of great importance is clearly the further development of the three mentioned methods, but also the finding of novel techniques which will allow the analysis of the actual cell metabolism of host cell and pathogen under in vivo infection conditions.

To achieve this goal, it is equally important to introduce genuine primary host cells, tissue and organoid systems as well as suitable animal models for the analysis of the crucial metabolic processes that occur in the host cell and the pathogen during infections. Only armed with this knowledge, we can expect to find metabolic targets for novel drugs that are of therapeutic value in the fight against diseases caused by microbial pathogens. While this article was in the final reviewing phase, a review was published by A. Best and Y. Abu Kwaik Trends Microbiol Jan The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Abshire, C. MTOR-driven metabolic reprogramming regulates Legionella pneumophila intracellular niche homeostasis. PLoS Pathog. Abu Kwaik, Y. Host delivery of favorite meals for intracellular pathogens.

Adams, O. Ahmed, D. Role of cellular metabolism in regulating type I interferon responses: implications for tumour immunology and treatment. Cancer Lett. Alkhuder, K. Glutathione provides a source of cysteine essential for intracellular multiplication of Francisella tularensis. Allonso, D. Dengue Virus NS1 protein modulates cellular energy metabolism by increasing glyceraldehydephosphate dehydrogenase activity. Aloni-Grinstein, R. Cancers Basel.

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Metabolic reprogramming by viruses in the sunlit and dark ocean

Al-Zeer, M. EBioMedicine 23, — Anderson, M. Shigella diversity and changing landscape: insights for the twenty-first century.