Streptococcus pyogenes upregulates arginine catabolism to exert its pathogenesis on the skin surface

The arginine deiminase (ADI) pathway has been found in many kinds of bacteria and functions to supplement energy production and provide protection against acid stress. The Streptococcus pyogenes ADI pathway is upregulated upon exposure to various environmental stresses, including glucose starvation. However, there are several unclear points about the advantages to the organism for upregulating arginine catabolism. We show that the ADI pathway contributes to bacterial viability and pathogenesis under low-glucose conditions. S. pyogenes changes global gene expression, including upregulation of virulence genes, by catabolizing arginine. In a murine model of epicutaneous infection, S. pyogenes uses the ADI pathway to augment its pathogenicity by increasing the expression of virulence genes, including those encoding the exotoxins. We also find that arginine from stratum-corneum-derived filaggrin is a key substrate for the ADI pathway. In summary, arginine is a nutrient source that promotes the pathogenicity of S. pyogenes on the skin.

Automated summary

The ADI pathway in Streptococcus pyogenes enhances bacterial survival and pathogenicity under low-glucose conditions by altering gene expression, particularly by upregulating virulence genes. By increasing the expression of virulence genes, including those encoding exotoxins, S. pyogenes augments its pathogenicity through the ADI pathway. Furthermore, arginine from filaggrin in the stratum corneum serves as a key substrate for the ADI pathway, promoting the pathogenicity of S. pyogenes on the skin.