Dataset Information

The Response and Survival Mechanisms of Staphylococcus aureus under High Salinity Stress in Salted Foods.

ABSTRACT: Staphylococcus aureus (S. aureus) has a strong tolerance to high salt stress. It is a major reason as to why the contamination of S. aureus in salted food cannot be eradicated. To elucidate its response and survival mechanisms, changes in the morphology, biofilm formation, virulence, transcriptome, and metabolome of S. aureus were investigated. IsaA positively regulates and participates in the formation of biofilm. Virulence was downregulated to reduce the depletion of nonessential cellular functions. Inositol phosphate metabolism was downregulated to reduce the conversion of functional molecules. The MtsABC transport system was downregulated to reduce ion transport and signaling. Aminoacyl-tRNA biosynthesis was upregulated to improve cellular homeostasis. The betaine biosynthesis pathway was upregulated to protect the active structure of proteins and nucleic acids. Within a 10% NaCl concentration, the L-proline content was upregulated to increase osmotic stability. In addition, 20 hub genes were identified through an interaction analysis. The findings provide theoretical support for the prevention and control of salt-tolerant bacteria in salted foods.

SUBMITTER: Feng Y

PROVIDER: S-EPMC9140498 | biostudies-literature | 2022 May

REPOSITORIES: biostudies-literature

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The Response and Survival Mechanisms of Staphylococcus aureus under High Salinity Stress in Salted Foods.

Feng Ying Y Ming Tinghong T Zhou Jun J Lu Chenyang C Wang Rixin R Su Xiurong X

Foods (Basel, Switzerland) 20220522 10

Staphylococcus aureus (S. aureus) has a strong tolerance to high salt stress. It is a major reason as to why the contamination of S. aureus in salted food cannot be eradicated. To elucidate its response and survival mechanisms, changes in the morphology, biofilm formation, virulence, transcriptome, and metabolome of S. aureus were investigated. IsaA positively regulates and participates in the formation of biofilm. Virulence was downregulated to reduce the depl ...[more]

PMID: 35627073

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Project description:Staphylococcus aureus is an important human commensal and opportunistic pathogen responsible for a wide range of infections. Long chain unsaturated free fatty acids represent a barrier to colonisation and infection by S. aureus and act as an antimicrobial component of the innate immune system where they are found on epithelial surfaces and in abscesses. Despite many contradictory reports, the precise anti-staphylococcal mode of action of free fatty acids remains undetermined. In this study, transcriptional (microarrays and qRT-PCR) and translational (proteomics) analyses were applied to ascertain the response of S. aureus to a range of free fatty acids. An increase in expression of the sigma(B) and CtsR stress response regulons was observed. This included increased expression of genes associated with staphyloxanthin synthesis, which has been linked to membrane stabilisation. Similarly, up-regulation of genes involved in capsule formation was recorded as were significant changes in the expression of genes associated with peptidoglycan synthesis and regulation. Overall, alterations were recorded predominantly in pathways involved in cellular energetics. In addition, sensitivity to linoleic acid of a range of defined (sigB, arcA, sasF, sarA, agr, crtM) and transposon-derived mutants (vraE, SAR2632) was determined. Taken together, these data indicate a common mode of action for long chain unsaturated fatty acids that involves disruption of the cell membrane, leading to interference with energy production within the bacterial cell. Contrary to data reported for other strains, the clinically important EMRSA-16 strain MRSA252 used in this study showed an increase in expression of the important virulence regulator RNAIII following all of the treatment conditions tested. An adaptive response by S. aureus of reducing cell surface hydrophobicity was also observed. Two fatty acid sensitive mutants created during this study were also shown to diplay altered pathogenesis as assessed by a murine arthritis model. Differences in the prevalence and clinical importance of S. aureus strains might partly be explained by their responses to antimicrobial fatty acids.

Project description:Periprosthetic joint infection (PJI) occurring after artificial joint replacement is a major clinical issue requiring multiple surgeries and antibiotic interventions. Staphylococcus aureus is the bacterium most commonly responsible for PJI. Recent in vitro research has shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid (SF). We hypothesize that these aggregates provide early protection to bacteria entering the wound site, allowing them time to attach to the implant surface, leading to biofilm formation. Thus, understanding the attachment kinetics of these aggregates is critical in understanding their adhesion to various biomaterial surfaces. In this study, the number, size, and surface area coverage of aggregates as well as of single cells of S. aureus were quantified under various conditions on different orthopedic materials relevant to orthopedic surgery: stainless steel (316L), titanium (Ti), hydroxyapatite (HA), and polyethylene (PE). It was observed that, regardless of the material type, SF-induced aggregation resulted in reduced aggregate surface attachment and greater aggregate size than the single-cell populations under various shear stresses. Additionally, the surface area coverage of bacterial aggregates on PE was relatively high compared to that on other materials, which could potentially be due to the rougher surface of PE. Furthermore, increasing shear stress to 78 mPa decreased aggregate attachment to Ti and HA while increasing the aggregates' average size. Therefore, this study demonstrates that SF induced inhibition of aggregate attachment to all materials, suggesting that biofilm formation is initiated by lodging of aggregates on the surface features of implants and host tissues.IMPORTANCE Periprosthetic joint infection occurring after artificial joint replacement is a major clinical issue that require repeated surgeries and antibiotic interventions. Unfortunately, 26% of patients die within 5 years of developing these infections. Staphylococcus aureus is the bacterium most commonly responsible for this problem and can form biofilms to provide protection from antibiotics as well as the immune system. Although biofilms are evident on the infected implants, it is unclear how these are attached to the surface in the first place. Recent in vitro investigations have shown that staphylococcal strains rapidly form aggregates in the presence of synovial fluid and provide protection to bacteria, thus allowing them time to attach to the implant surface, leading to biofilm formation. In this study, we investigated the attachment kinetics of Staphylococcus aureus aggregates on different orthopedic materials. The information presented in this article will be useful in surgical management and implant design.

Dataset Information

The Response and Survival Mechanisms of Staphylococcus aureus under High Salinity Stress in Salted Foods.

Publications

The Response and Survival Mechanisms of <i>Staphylococcus aureus</i> under High Salinity Stress in Salted Foods.

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