Dinner date: Neisseria gonorrhoeae central carbon metabolism and pathogenesis

Abstract

Neisseria gonorrhoeae, the causative agent of the sexually transmitted infection gonorrhea, is a human-adapted pathogen that does not productively infect other organisms. The ongoing relationship between N. gonorrhoeae and the human host is facilitated by the exchange of nutrient resources that allow for N. gonorrhoeae growth in the human genital tract. What N. gonorrhoeae ‘eats' and the pathways used to consume these nutrients have been a topic of investigation over the last 50 years. More recent investigations are uncovering the impact of N. gonorrhoeae metabolism on infection and inflammatory responses, the environmental influences driving N. gonorrhoeae metabolism, and the metabolic adaptations enabling antimicrobial resistance. This mini-review is an introduction to the field of N. gonorrhoeae central carbon metabolism in the context of pathogenesis. It summarizes the foundational work used to characterize N. gonorrhoeae central metabolic pathways and the effects of these pathways on disease outcomes, and highlights some of the most recent advances and themes under current investigation. This review ends with a brief description of the current outlook and technologies under development to increase understanding of how the pathogenic potential of N. gonorrhoeae is enabled by metabolic adaptation.

Chlamydia trachomatis and Neisseria gonorrhoeae rectal infections: Interplay between rectal microbiome, HPV infection and Torquetenovirus

“…The inflammatory environment triggered by chlamydial/gonococcal infections could perturb the homeostasis of the rectal bacterial communities, leading to the proliferation/ depletion of specific genera [31,32]. In addition, the nutritional requirements of CT and NG could alter specific metabolic pathways, enabling the preferential replication of some bacterial genera compared to others [34,35].…”

Nondigestible carbohydrates and gut microbiota: A dynamic duo in host defense

“…To detect ambient acetate, intestinal enterocytes and other cell types contain G-protein-coupled receptors, which mediate most of the molecular effects of acetate (Hosmer et al 2023). One example is the fact that oral acetate may upregulate IFN-stimulated genes in the lung, leading to interferon-β (IFN-β) responses (Antunes et al 2019).…”

Optimal Protein Allocation Controls the Inhibition of GltA and AcnB inNeisseria gonorrhoeae

“…Despite having the ability to encode a complete tricarboxylic acid (TCA) cycle, previous studies revealed Ngo's puzzling phenotype of restricting crucial TCA cycle enzymes, such as GltA and AcnB (Potter and Criss 2023a).Additionally, it does not have the ability to encode phosphofructokinase (PFK). To probe deeper into metabolic anomaly in the TCA cycle, the application of systems biology, particularly, genome-scale metabolic models (GEMs), provides a promising avenue, since it has been proven to answer unusual bacterial phenomena (Chowdhury et al 2023).…”

“…Despite having the ability to encode a complete tricarboxylic acid (TCA) cycle, previous studies revealed Ngo’s puzzling phenotype of restricting crucial TCA cycle enzymes, such as GltA and AcnB (Potter and Criss 2023a). Additionally, it does not have the ability to encode phosphofructokinase (PFK).…”