4.6 Article

Antimicrobial and anti-biofilm potencies of dermcidin-derived peptide DCD-1L against Acinetobacter baumannii: an in vivo wound healing model

Journal

BMC MICROBIOLOGY
Volume 22, Issue 1, Pages -

Publisher

BMC
DOI: 10.1186/s12866-022-02439-8

Keywords

Acinetobacter baumannii; Antimicrobial peptide; Biofilms; Dermcidin-1L; Wound healing

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Funding

  1. Ahvaz Jundishapur University of Medical Sciences [IR.AJUMR.REC.1397.861]

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The study showed that DCD-1L can effectively inhibit adhesion and biofilm formation of Acinetobacter baumannii, reducing the likelihood of infection. DCD-1L also accelerates the process of re-epithelialization of wounds, making it a promising candidate for antimicrobial and anti-biofilm drug development.
Background The global emergence of Acinetobacter baumannii resistance to most conventional antibiotics presents a major therapeutic challenge and necessitates the discovery of new antibacterial agents. The purpose of this study was to investigate in vitro and in vivo anti-biofilm potency of dermcidin-1L (DCD-1L) against extensively drug-resistant (XDR)-, pandrug-resistant (PDR)-, and ATCC19606-A. baumannii. Methods After determination of minimum inhibitory concentration (MIC) of DCD-1L, in vitro anti-adhesive and anti-biofilm activities of DCD-1L were evaluated. Cytotoxicity, hemolytic activity, and the effect of DCD-1L treatment on the expression of various biofilm-associated genes were determined. The inhibitory effect of DCD-1L on biofilm formation in the model of catheter-associated infection, as well as, histopathological examination of the burn wound sites of mice treated with DCD-1L were assessed. Results The bacterial adhesion and biofilm formation in all A. baumannii isolates were inhibited at 2 x , 4 x , and 8 x MIC of DCD-1L, while only 8 x MIC of DCD-1L was able to destroy the pre-formed biofilm in vitro. Also, reduce the expression of genes involved in biofilm formation was observed following DCD-1L treatment. DCD-1L without cytotoxic and hemolytic activities significantly reduced the biofilm formation in the model of catheter-associated infection. In vivo results showed that the count of A. baumannii in infected wounds was significantly decreased and the promotion in wound healing by the acceleration of skin re-epithelialization in mice was observed following treatment with 8 x MIC of DCD-1L. Conclusions Results of this study demonstrated that DCD-1L can inhibit bacterial attachment and biofilm formation and prevent the onset of infection. Taking these properties together, DCD-1L appears as a promising candidate for antimicrobial and anti-biofilm drug development.

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