Infection-elicited microbiota promotes host adaptation to nutrient restriction

Abstract

The microbiota performs multiple functions vital to host fitness, including defense against pathogens and adaptation to dietary changes. Yet, how environmental challenges shape microbiota resilience to nutrient fluctuation remains largely unexplored. Here, we show that transient gut infection can optimize host metabolism toward the usage of carbohydrates. Following acute infection and clearance of the pathogen, mice gained more weight as a result of white adipose tissue expansion. Concomitantly, previously infected mice exhibited enhanced carbohydrate (glucose) disposal and insulin sensitivity. This metabolic remodeling depended on alterations to the gut microbiota, with infection-elicited Betaproteobacteria being sufficient to enhance host carbohydrate metabolism. Further, infection-induced metabolic alteration protected mice against stunting in the context of limited nutrient availability. Together, these results propose that alterations to the microbiota imposed by acute infection may enhance host fitness and survival in the face of nutrient restriction, a phenomenon that may be adaptive in settings where both infection burden and food precarity are prevalent.

13 C metabolite tracing reveals glutamine and acetate as critical in vivo fuels for CD8 T cells

“…S6A). Acetate levels have been reported to peak at sites of inflammation and are also produced by the microbiome (59)(60)(61), which may dictate the preferential use of acetate by T cells simply by being readily available. Alternatively, changes in glutamine availability may dictate the switch to acetate oxidation.…”

SARS‐CoV‐2, periodontal pathogens, and host factors: The trinity of oral post‐acute sequelae of COVID‐19

“…In this context, metabolites produce nutrients that sustain and support the survival of some bacterial pathogens while acting as a bactericide to some non‐pathogenic bacteria. Notably, these altered bacterial metabolic processes can result in the synthesis of sulfides or ROS, including nitrite, nitric oxide, or nitrosyl radicals, with implications for pathogen competition and potential dysbiosis 189,190 …”

“…Notably, these altered bacterial metabolic processes can result in the synthesis of sulfides or ROS, including nitrite, nitric oxide, or nitrosyl radicals, with implications for pathogen competition and potential dysbiosis. 189,190 Once pathogens have adhered to receptors on oral epithelial cells or membrane adhesion molecules, such as glycosaminoglycans, phospholipids, metalloproteins, they initiate processes that involve the synthesis of specific proteins, such as FAD-1. FAD-1 associates with F. nucleatum and is linked to alterations in phospholipidphospholipase-diacylglycerol dynamics, as well as the activation of protein kinase C. This intracellular molecular reorganization is coordinated with the pathogen's inward movement, propelling it around the oral epithelial cell while simultaneously releasing defensin.…”