L-arginine metabolism as pivotal interface of mutual host–microbe interactions in the gut

ABSTRACT

L-arginine (L-arg) is a versatile amino acid and a central intestinal metabolite in mammalian and microbial organisms. Thus, L-arg participates as precursor of multiple metabolic pathways in the regulation of cell division and growth. It also serves as a source of carbon, nitrogen, and energy or as a substrate for protein synthesis. Consequently, L-arg can simultaneously modify mammalian immune functions, intraluminal metabolism, intestinal microbiota, and microbial pathogenesis. While dietary intake, protein turnover or de novo synthesis usually supply L-arg in sufficient amounts, the expression of several key enzymes of L-arg metabolism can change rapidly and dramatically following inflammation, sepsis, or injury. Consequently, the availability of L-arg can be restricted due to increased catabolism, transforming L-arg into an essential amino acid. Here, we review the enzymatic pathways of L-arg metabolism in microbial and mammalian cells and their role in immune function, intraluminal metabolism, colonization resistance, and microbial pathogenesis in the gut.

KEYWORDS:

• L-arginine (L-arg)
• intestinal microbiota
• mucosal immune function
• microbial pathogenesis
• mutual metabolic pathways
• colonization resistance
• host–microbe interaction
• virulence factor
• dietary L-arg supplementation

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

All data analyzed during this study are included in this published article.

Additional information

Funding

The German Research Foundation (DFG-CRC1181-project number C04 and DFG-MA 2621/5-1), Sino German Center Mobility Programme M–693, the Staedtler Stiftung, the Sino-German Center Mobility Programme (M-0693), and the Johannes and Frieda Marohn Stiftung supported this research.