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Citation
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HERO ID
2883811
Reference Type
Journal Article
Title
Staphylococcus epidermidis saeR is an effector of anaerobic growth and a mediator of acute inflammation
Author(s)
Handke, LD; Rogers, KL; Olson, ME; Somerville, GA; Jerrells, TJ; Rupp, AE; Dunman, PA; Fey, PD
Year
2008
Is Peer Reviewed?
Yes
Journal
Infection and Immunity
ISSN:
0019-9567
EISSN:
1098-5522
Volume
76
Issue
1
Page Numbers
141-152
Language
English
PMID
17954724
DOI
10.1128/IAI.00556-07
Web of Science Id
WOS:000252126000015
Abstract
The saeRS two-component regulatory system regulates transcription of multiple virulence factors in Staphylococcus aureus. In the present study, we demonstrated that the saePQRS region in Staphylococcus epidermidis is transcriptionally regulated in a temporal manner and is arranged in a manner similar to that previously described for S. aureus. Studies using a mouse foreign body infection model demonstrated that the virulence of strain 1457 and the virulence of a mutant, strain 1457 saeR, were statistically equivalent. However, histological analyses suggested that the polymorphonuclear neutrophil response at 2 days postinfection was significantly greater in 1457-infected mice than in 1457 saeR-infected mice, demonstrating that SaeR influences the early, acute phases of infection. Microarray analysis demonstrated that a saeR mutation affected the transcription of 65 genes (37 genes were upregulated and 28 genes were downregulated); in particular, 8 genes that facilitate growth under anaerobic conditions were downregulated in 1457 saeR. Analysis of growth under anaerobic conditions demonstrated that 1457 saeR had a decreased growth rate compared to 1457. Further metabolic experiments demonstrated that 1457 saeR had a reduced capacity to utilize nitrate as a terminal electron acceptor and exhibited increased production of lactic acid in comparison to 1457. These data suggest that in S. epidermidis SaeR functions to regulate the transition between aerobic growth and anaerobic growth. In addition, when grown anaerobically, 1457 saeR appeared to compensate for the redox imbalance created by the lack of electron transport-mediated oxidation of NADH to NAD+ by increasing lactate dehydrogenase activity and the subsequent oxidation of NADH.
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Nitrate/Nitrite
Supplemental LitSearch Update 1600-2015
PubMed
WoS
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