Amino acid decarboxylase-dependent acid tolerance, selected phenotypic, and virulence gene expression responses of Salmonella enterica serovar Heidelberg

- S. Heidelberg can establish acid tolerance response after mild acid adaptation.
- Lysine and arginine addition improved S. Heidelberg extreme acid survival.
- Arginine and lysine decarboxylase genes were induced in acid environment in 1 h.
- Acid adaptation improved S. Heidelberg swim ability and enterotoxin gene expression.

Salmonella enterica serovar Heidelberg (S. Heidelberg) is one of the pathogens most frequently detected in recent years in food products from animals; here, we examine the acid tolerance of this strain. Mild acid (pH 5.5-5.0) induced a strong acid resistance in S. Heidelberg; the induced acid resistance improved within 0.5-6 h and resulted in > 95% cell survival following challenge in pH 3.0 medium. Addition of lysine or arginine to pH 2.5 acid challenge medium significantly improved the survival of S. Heidelberg; lysine induced the largest increase in survival. The lysine and arginine decarboxylase-related genes (i.e., cadA, cadB, adiA, and adiY) are acid induced genes, and they play an important role in S. Heidelberg acid resistance. RT-PCR showed that the genes expression levels increased as acid adaptation pH decreased. The increased expression was maintained for at least 4 h during adaptation. Moreover, acid adaptation may have increased the production of cellulose and swimming in S. Heidelberg; pH 5.5 acid-adapted cells showed a red, dry, and rough morphotype on Congo red plates. The transcriptional levels of Enterotoxin gene (stn) increased three times following acid adaptation; however, the expression of Salmonella pathogenicity island 1 virulence genes significantly decreased.

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