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Review
. 2019 Jul 16:8:118.
doi: 10.1186/s13756-019-0559-6. eCollection 2019.

Review on plant antimicrobials: a mechanistic viewpoint

Affiliations
Review

Review on plant antimicrobials: a mechanistic viewpoint

Bahman Khameneh et al. Antimicrob Resist Infect Control. .

Abstract

Microbial resistance to classical antibiotics and its rapid progression have raised serious concern in the treatment of infectious diseases. Recently, many studies have been directed towards finding promising solutions to overcome these problems. Phytochemicals have exerted potential antibacterial activities against sensitive and resistant pathogens via different mechanisms of action. In this review, we have summarized the main antibiotic resistance mechanisms of bacteria and also discussed how phytochemicals belonging to different chemical classes could reverse the antibiotic resistance. Next to containing direct antimicrobial activities, some of them have exerted in vitro synergistic effects when being combined with conventional antibiotics. Considering these facts, it could be stated that phytochemicals represent a valuable source of bioactive compounds with potent antimicrobial activities.

Keywords: Antibiotic-resistant; Antimicrobial activity; Combination therapy; Mechanism of action; Natural products; Phytochemicals.

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Conflict of interest statement

Competing interestsThe authors declare that they have no competing interests.

Figures

Fig. 1
Fig. 1
a Proven targets for antibacterial drugs. Protein biosynthesis at the ribosome is targeted by different classes of antibiotics such as macrolides, tetracyclines, aminoglycosides. Cell membrane can be targeted by some antibiotics such as Polymyxin B. These antibiotics alter bacterial outer membrane permeability and finally destabilize outer membrane of bacteria. The fluoroquinolone antibiotics inhibit DNA replication by trapping a complex of DNA bound to the enzyme DNA Gyrase. Cell-wall biosynthesis is inhibited by the various classes of antibiotics. b Multiple antibiotic resistance mechanisms in bacteria. Efflux pumps remove the antibiotics from bacteria (e.g. Fluoroquinolones and trimethoprim resistance in P. aeruginosa). Destruction enzymes that degrade the antibiotics (β-lactams in Enterobacteriaceae). Modifying enzymes which change the antibiotic structure (e.g. chloramphenicol or fosfomycin in P. aeruginosa)
Fig. 2
Fig. 2
Schematic representation of the main families of bacterial efflux pumps. The resistance- nodulation-division (RND) family, the small multidrug resistance (SMR) family, the major facilitator superfamily (MFS), the multidrug and toxic compound extrusion (MATE) family and the adenosine triphosphate (ATP)-binding cassette (ABC) superfamily
Fig. 3
Fig. 3
Chemical structures of selected antimicrobial alkaloids
Fig. 4
Fig. 4
Chemical structures of selected antimicrobial organosulfur compounds
Fig. 5
Fig. 5
Chemical structures of selected antimicrobial phenolic compounds
Fig. 6
Fig. 6
Chemical structures of selected antimicrobial coumarins
Fig. 7
Fig. 7
Chemical structures of selected antimicrobial terpenes

References

    1. WHO G . WHO methods and data sources for global burden of disease estimates 2000–2011. Geneva: Department of Health Statistics and Information Systems; 2013.
    1. Gupta M, Sharma R, Kumar A. Comparative potential of simvastatin, Rosuvastatin and Fluvastatin against bacterial infection: an in silico and in vitro study. Orient Pharm Exp Med. 2019:1–17. 10.1007/s13596-019-00359-z.
    1. WHO . Antimicrobial resistance: Global report on surveillance. Geneva: WHO; 2014.
    1. Baym M, Stone LK, Kishony R. Multidrug evolutionary strategies to reverse antibiotic resistance. Science. 2016;351(6268):aad3292. doi: 10.1126/science.aad3292. - DOI - PMC - PubMed
    1. Brown D. Antibiotic resistance breakers: can repurposed drugs fill the antibiotic discovery void? Nat Rev Drug Discov. 2015;14(12):821–832. doi: 10.1038/nrd4675. - DOI - PubMed

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