New Insights Toward the Development of Novel Inhibitors of S. aureus and P. aeruginosa Factors

Dear Colleagues,

Staphylococcus aureus and Pseudomonas aeruginosa, both classified among the ESKAPE pathogens, represent a growing public health concern due to their increasing multidrug resistance and the limited development of new antimicrobial therapies. P. aeruginosa possesses three interconnected quorum-sensing (QS) circuits regulated by MvfR, LasR, and RhlR, which are central to P. aeruginosa’ s virulence and antibiotic resistance mechanisms. MvfR (formerly known as PqsR) is a major regulator of multiple P. aeruginosa virulence factors and plays a crucial role in acute, persistent, and relapsing infections. MvfR influences the expressions of LasR and RhlR, and both contribute to P. aeruginosa’ s competition with other microbes via the production of siderophores (pyoverdine, pyochelin) and phenazines (pyocyanin). RhlR directly regulates P. aeruginosa virulent factor rhamnolipids. S. aureus infections pose a significant challenge due to the involved virulence factors and increasing antibiotic resistance. S. aureus utilizes surface proteins to bind host cells and tissues or employs protein A to bind to antibodies and block the host’s immune response. S. aureus secretes various toxins that cause tissue destruction and systemic toxicity, and it forms biofilms that act as a protective barrier against antibiotics and the host immune system. A coinfection with S. aureus and P. aeruginosa increases severity and complications in patients with cystic fibrosis, wound infections, and respiratory infections. The coexistence of S. aureus and P. aeruginosa can increase antibiotic resistance due to a mix of biofilms, an enhanced tolerance to certain antibiotics, and an altered pattern of gene expression leading to an increase in the expression of genes associated with antibiotic resistance. This Special Issue seeks manuscript submissions that further our understanding of antimicrobial resistance in the coinfection of S. aureus and P. aeruginosa, as well as new approaches toward the development of novel strategies to inhibit S. aureus and P. aeruginosa components. Contributions on combination therapy, anti-biofilm strategies, or targeting microbial interactions and host response are especially encouraged.

Dr. Que Chi Truong-Bolduc
Dr. Leon G. Leanse
Prof. Dr. Hidemasa Nakaminami
Dr. Chun-Hsing Liao
Guest Editors

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• MSSA
• MRSA
• P. aeruginosa
• coinfection
• antibiotic resistance
• therapeutic strategy
• anti-virulence
• quorum-sensing
• virulence factors
• biofilms