Staphylococcus aureus (S. aureus), a leading cause of nosocomial infections, contributes significantly to increased morbidity and mortality, especially when it forms biofilms on medical devices. This pathogen, specifically methicillin-resistant S. aureus (MRSA), remains a challenge to treat due to its ability to form biofilms and rapidly develop resistance against antibiotics. Biofilm formation allows bacteria to adhere to biotic and abiotic surfaces, creating a protective matrix that shields them from immune responses and antibiotic therapies. The widespread prevalence of multidrug-resistant S. aureus biofilms poses a significant therapeutic challenge in clinical settings. Several novel therapeutic strategies have been developed to combat S. aureus biofilm-associated infections. Accumulating evidence suggests that natural plants and their derivatives possess antimicrobial and chemo preventive properties that can disrupt established biofilms. Several plant-derived compounds with anti-biofilm activities have been reported to target the regulatory proteins involved in the Agr quorum sensing (Agr-QS) system, underscoring their potential as therapeutic candidates for the prevention and treatment of biofilm-associated infections. However, despite these encouraging findings, clinical validation of these plant-based agents is essential to ensure their efficacy, safety, and optimal application in treating S. aureus biofilm infections. The continued exploration of natural biofilm inhibitors anticipates the urgent need for new treatments to combat biofilm-associated infections and multidrug-resistant pathogens like MRSA. This review provides a detailed overview of preventive and therapeutic interventions to eradicate biofilm-forming S. aureus infections.
Salma Waheed Sheikh, Ahmad Ali, A. Ahsan et al.· Pathogens· 0 citations
Staphylococcus aureus (S. aureus) is a major Gram-positive pathogen capable of sensing and responding to diverse host- and environment-derived stresses, contributing to both clinical infections and foodborne illnesses. This exceptional stress tolerance is primarily mediated by intricate regulatory networks. Although the ArlRS two-component system is known to regulate autolysis, capsule synthesis, and virulence, the specific role of ArlR in environmental stress adaptation remains poorly understood. In this study, we demonstrate that deletion of arlR significantly reduces the tolerance of the foodborne strain RMSA49 to acetic acid, desiccation, whereas its responses to temperature and osmotic stress not affected. Notably, the arlR mutant also exhibits significantly enhanced biofilm formation. Transcriptomic analysis, validated by RT–qPCR, further reveals that ArlR regulates a broad set of stress- and biofilms-associated genes, highlighting its central role in coordinating environmental adaptation. These findings establish ArlR as a key regulator of environmental stress adaptation in foodborne S. aureus RMSA49 and suggest its potential as a target for controlling S. aureus.
Kai Ma, Bingtao Zhang, Xia-Yan Zhang et al.· Current Research in Food Sci...· 0 citations
Staphylococcus aureus is an important raw milk contaminant that can persist in dairy environments through biofilm formation and adaptation to environmental stresses. Although the alternative sigma factor SigH has been described in S. aureus, its role in raw milk-associated strains remains poorly understood. In this study, we investigated the function of SigH in the raw milk-derived S. aureus strain RMSA24 in biofilm formation, stress tolerance and antibiotic susceptibility. Deletion of sigH did not affect bacterial growth under routine culture conditions but significantly reduced biofilm formation. In contrast, the sigH mutant exhibited enhanced tolerance to osmotic, acid, and heat stresses. Loss of sigH also reduced susceptibility to the glycopeptide antibiotics vancomycin and teicoplanin and was accompanied by pronounced cell wall thickening. Transcriptomic analysis further supported these phenotypes by revealing differential expression of genes associated with biofilm formation, stress tolerance, and cell wall homeostasis. Overall, these findings indicate that SigH contributes to the regulation of persistence-associated phenotypes in a raw milk-derived S. aureus strain and provide new insights into the regulatory mechanisms that may influence survival of this pathogen in dairy-related environments.
Chao Li, Fanwenqing Kong, Wenting Li et al.· Journal of Dairy Science· 0 citations
Staphylococcus aureus has significantly contributed to the contamination of dairy products and preserved foods, attributed to its ability to colonize a wide range of environments and form biofilms. ArcR, the Crp/Fnr family regulatory protein in S. aureus plays key roles in various biological processes. However, the molecular mechanism underlying biofilm regulation by the cAMP-ArcRsa complex remains poorly defined. In this work, we investigated the biological function of ArcRsa in mediating biofilm formation in dairy-derived S. aureus RMSA49. The results demonstrated that the deletion of arcRsa resulted in a dramatic increase in biofilm formation. An in-depth dissection of the regulatory mechanism of ArcRsa revealed that it negatively regulates the production of the polysaccharide intercellular adhesin (PIA) by directly binding to the promoter of the gene icaA. Further analysis revealed that cAMP-ArcRsa complex support biofilm maintenance of S. aureus RMSA 49 by strengthening its regulation of genes icaA. ArcRsa controls the transcription of its own gene and icaA by attaching to specific sequences at the site arcRsa (5'-ATCACGCGACAA-3') and site arcRsa2 (5'-ATTAAGTTGCAA-3'). Our results demonstrate functional crosstalk between cAMP and ArcRsa through direct regulation at the gene icaA promoter, supporting an essential regulatory role for the cAMP-ArcRsa signaling module in modulating biofilm formation in S. aureus.
Haoyang He, Fanwenqing Kong, Xiaojia Xuan et al.· Journal of Dairy Science· 0 citations
We use cookies to run the site and, with your consent, for analytics and to show ads.
See our Cookie Policy.
