Kinetic analysis of PPi-dependent phosphofructokinase from<i>Porphyromonas gingivalis</i>

Arimoto, Takafumi; Ansai, Toshihiro; Yu, Weixian; Turner, Anthony J.; Takehara, Tadamichi

doi:10.1111/j.1574-6968.2002.tb11024.x

Cited by 7 publications

(1 citation statement)

References 26 publications

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“…Indeed, several IBPs ( Rickettsia, Chlamydia, Coxiella , and Legionella ) lack the typical bacterial type I-III fructose-1,6-diphosphatases (FBPase, an essential enzyme for gluconeogenesis). It is, however, possible that these IBPs, some of which (e.g., L. pneumophila ) are definitely able to perform gluconeogenesis, might compensate the missing conventional FBPase by alternative FBPase activities, e.g., by the reversible pyrophosphate-dependent phosphofructokinase or fructose-6-phosphate aldolase (Schürmann and Sprenger, 2001; Arimoto et al, 2002; Ganapathy et al, 2015). On the other hand, in Brucella abortus which possesses type I and type II FBPases, both enzymes are dispensible for intracellular replication (Zuniga-Ripa et al, 2014), whereas in Francisella tularensis inactivation of the glpX gene (encoding a type II FBPase) leads to reduced intracellular multiplication (Brissac et al, 2015), indicating the need of gluconeogenesis for intracellular replication of this IBP particularly in those stages of infection in which glucose is limited.…”

Section: Metabolic Adaptations Of Iis Cells and The Ibpsmentioning

confidence: 99%

To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection

Eisenreich

Rudel

Heesemann

et al. 2017

Front. Cell. Infect. Microbiol.

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Intracellular bacterial pathogens (IBPs) invade and replicate in different cell types including immune cells, in particular of the innate immune system (IIS) during infection in the acute phase. However, immune cells primarily function as essential players in the highly effective and integrated host defense systems comprising the IIS and the adaptive immune system (AIS), which cooperatively protect the host against invading microbes including IBPs. As countermeasures, the bacterial pathogens (and in particular the IBPs) have developed strategies to evade or reprogram the IIS at various steps. The intracellular replication capacity and the anti-immune defense responses of the IBP's as well as the specific antimicrobial responses of the immune cells of the innate and the AIS depend on specific metabolic programs of the IBPs and their host cells. The metabolic programs of the immune cells supporting or counteracting replication of the IBPs appear to be mutually exclusive. Indeed, recent studies show that upon interaction of naïve, metabolically quiescent immune cells with IBPs, different metabolic activation processes occur which may result in the provision of a survival and replication niche for the pathogen or its eradication. It is therefore likely that within a possible host cell population subsets exist that are metabolically programmed for pro- or anti-microbial conditions. These metabolic programs may be triggered by the interactions between different bacterial agonistic components and host cell receptors. In this review, we summarize the current status in the field and discuss metabolic adaptation processes within immune cells of the IIS and the IBPs that support or restrict the intracellular replication of the pathogens.

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Section: Metabolic Adaptations Of Iis Cells and The Ibpsmentioning

confidence: 99%

To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection

Eisenreich

Rudel

Heesemann

et al. 2017

Front. Cell. Infect. Microbiol.

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The life stage‐specific pathometabolism of Legionella pneumophila

Eisenreich

Heuner

2016

FEBS Letters

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The genus Legionella belongs to Gram-negative bacteria found ubiquitously in aquatic habitats, where it grows in natural biofilms and replicates intracellularly in various protozoa (amoebae, ciliates). L. pneumophila is known as the causative agent of Legionnaires' disease, since it is also able to replicate in human alveolar macrophages, finally leading to inflammation of the lung and pneumonia. To withstand the degradation by its host cells, a Legionellacontaining vacuole (LCV) is established for intracellular replication, and numerous effector proteins are secreted into the host cytosol using a type four B secretion system (T4BSS). During intracellular replication, Legionella has a biphasic developmental cycle that alternates between a replicative and a transmissive form. New knowledge about the host-adapted and life stagedependent metabolism of intracellular L. pneumophila revealed a bipartite metabolic network with life stage-specific usages of amino acids (e.g. serine), carbohydrates (e.g. glucose) and glycerol as major substrates. These metabolic features are associated with the differentiation of the intracellular bacteria, and thus have an important impact on the virulence of L. pneumophila.

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Diphosphate-fructose-6-phosphate 1-phosphotransferase

Springer Handbook of Enzymes

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Kinetic analysis of PPi-dependent phosphofructokinase fromPorphyromonas gingivalis

Cited by 7 publications

References 26 publications

To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection

To Eat and to Be Eaten: Mutual Metabolic Adaptations of Immune Cells and Intracellular Bacterial Pathogens upon Infection

The life stage‐specific pathometabolism of Legionella pneumophila

Diphosphate-fructose-6-phosphate 1-phosphotransferase

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