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Abstract
Here, we investigate the transcriptome profiles of two S. Enteritidis and one S. Schwarzengrund isolates that present different persister levels when exposed to ciprofloxacin or ceftazidime. It was possible to note a distinct transcript profile among isolates, time of exposure, and treatment. We could not find a commonly expressed transcript profile that plays a role in persister formation after S. enterica exposure to beta-lactam or fluoroquinolone, as only three DEGs presented the same behavior under the conditions and isolates tested. It appears that the formation of persisters in S. enterica after exposure to ciprofloxacin is linked to the overexpression of genes involved in the SOS response (recA), cell division inhibitor (sulA), iron-sulfur metabolism (hscA and iscS), and type I TA system (tisB). On the other hand, most genes differentially expressed in S. enterica after exposure to ceftazidime appeared to be downregulated and were part of the flagellar assembly apparatus, citrate cycle (TCA cycle), glycolysis/gluconeogenesis, carbon metabolism, bacterial secretion system, quorum sensing, pyruvate metabolism pathway, and biosynthesis of secondary metabolites. The different transcriptome profiles found in S. enterica persisters induced by ciprofloxacin and ceftazidime suggest that these cells modulate their response differently according to each stress.
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1 Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Laboratório de Imunologia e Microbiologia, Escola de Ciências da Saúde e da Vida, Porto Alegre, Brazil (GRID:grid.412519.a) (ISNI:0000 0001 2166 9094); Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Programa de Pós-Graduação em Biologia Celular e Molecular, Escola de Ciências da Saúde e da Vida, Porto Alegre, Brazil (GRID:grid.412519.a) (ISNI:0000 0001 2166 9094); The University of Tennessee Southern, UTS, College of Mathematics and Science, Pulaski, USA (GRID:grid.462503.6) (ISNI:0000 0004 0588 5477); South Dakota State University, SDSU, Department of Veterinary and Biomedical Sciences, Brookings, USA (GRID:grid.263791.8) (ISNI:0000 0001 2167 853X)
2 Universidade Federal de Ciências da Saúde de Porto Alegre (UFCSPA), Laboratório de Imunoterapia, Porto Alegre, Brazil (GRID:grid.412344.4) (ISNI:0000 0004 0444 6202)
3 South Dakota State University, SDSU, Department of Veterinary and Biomedical Sciences, Brookings, USA (GRID:grid.263791.8) (ISNI:0000 0001 2167 853X); Oklahoma State University, Department of Veterinary Pathobiology, Stillwater, USA (GRID:grid.65519.3e) (ISNI:0000 0001 0721 7331)
4 Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Laboratório de Imunologia e Microbiologia, Escola de Ciências da Saúde e da Vida, Porto Alegre, Brazil (GRID:grid.412519.a) (ISNI:0000 0001 2166 9094); Pontifícia Universidade Católica do Rio Grande do Sul, PUCRS, Programa de Pós-Graduação em Biologia Celular e Molecular, Escola de Ciências da Saúde e da Vida, Porto Alegre, Brazil (GRID:grid.412519.a) (ISNI:0000 0001 2166 9094)