Abstract
An increase in antibiotic resistance has led to escalating the need for the development of alternate therapy. Antimicrobial peptides (AMPs) are at the forefront of replacing conventional antibiotics, showing slower development of drug resistance, antibiofilm activity, and the ability to modulate the host immune response. The ESKAPE (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species) pathogens that jeopardize most conventional antibiotics are known to be involved in severe respiratory tract, bloodstream, urinary tract, soft tissue, and skin infections. Among them, S. aureus is an insidious microbe and developed resistance against conventional antibiotics. In the present study, an AMP (named as peptide-Ba49) isolated from Bacillus subtilis subsp. spizizenii strain from Allium cepa (the common onion) exhibited strong antibacterial efficacy against S. aureus ATCC 25923. The mode of action of this peptide-Ba49 on S. aureus was deciphered through various sensitive probes, i.e., DiSC3 (5) and H2DCFDA, suggesting the peptide-Ba49 to be acting upon through change in membrane potential and by triggering the production of reactive oxygen species (ROS). This induced disruption of the cell membrane was further supported by morphological studies using scanning electron microscopy (SEM). Investigations on a possible post-antibiotic effect (PAE) of peptide-Ba49 showed prolonged PAE against S. aureus. Furthermore, the peptide-Ba49 prevented the formation of S. aureus biofilm at low concentration and showed its potential to degrade the mature biofilm of S. aureus. The peptide-Ba49 also exhibited intracellular killing potential against S. aureus ATCC 25923 in the macrophage cells, and moreover, peptide-Ba49 was found to bolster the fibroblast cell migration in the scratch assay at low concentration, exhibiting a wound healing efficacy of this peptide. These studies demonstrated that peptide-Ba49 isolated from the strain B. subtilis subsp. spizizenii could be a therapeutic candidate to combat the pathogenic S. aureus infections.
Highlights
The expeditious emergence of bacterial resistance toward conventional antibiotics, especially those related to staphylococcal infections, has become a serious healthcare concern worldwide (Mohamed et al, 2016)
In the case of 4 h post-exposure at 2× minimum inhibitory concentration (MIC), the regrowth of the S. aureus cells was observed to be less as compared to post 2 h treatment at 2× MIC. These results indicated that higher cellular damage occurred within the S. aureus cells following 4 h of treatment of cells at 2× MIC of peptide-Ba49
The alarming factor related to S. aureus infection is their capability to form biofilm and become highly resistant to host attacks and antimicrobials (Lewis, 2001; Mah and O’toole, 2001; Savage et al, 2013; Koch et al, 2014)
Summary
The expeditious emergence of bacterial resistance toward conventional antibiotics, especially those related to staphylococcal infections, has become a serious healthcare concern worldwide (Mohamed et al, 2016). S. aureus is considered an extracellular pathogen, but its invasion ability plays a critical role in cases of pertinacious and chronic infection (Clement et al, 2005) It has the capability of causing skin and soft tissue infection, sepsis, mastitis, urinary tract infection, endocarditis, bone and joint infections, food poisoning, biofilm-associated infections, or septicemia (Lowy, 1998; Tong et al, 2015; Rollin et al, 2017). Infections like bacteremia and skin abscesses are generally caused by planktonic S. aureus cells by producing secreted toxins and exo-enzymes, whereas chronic infections are associated with S. aureus biofilm (Gordon and Lowy, 2008) This organism attaches and recurs on host tissues such as bone and heart valves causing osteomyelitis and endocarditis, respectively, and on implanted materials like pacemakers, prosthetic joints, etc. During the implantation of medical devices or biomaterials within the host, the host proteins such as fibronectin, fibrinogen, or fibrin coat these implants and become a potential target of interaction with the matrix-binding proteins present on the surface of S. aureus, leading to the formation of biofilm on these implants (Cheung and Fischetti, 1990; Francois et al, 1996)
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