Advanced Therapeutic Dressings for Effective Wound Healing—A Review

Background Acetaminophen (APAP) and ibuprofen (IB) are drugs commonly used to alleviate pain due to their anti-inflammatory, anti-pyretic, and analgesic effect. The aim of the present study is to unravel the molecular mechanisms underlying the antimicrobial potential of these two drugs against red complex pathogens, namely, Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, by using in silico tools, since they are potentially associated with inflammatory conditions related to periodontal infections. Methods The STITCH v5.0 pipeline was primarily used for identifying drug-protein interactions; VirulentPred and VICMPred were used for elucidating the virulence property and functional class of the proteins. The subcellular localization of virulent proteins was assessed using PSORTb v3.0 and the epitopes were identified using BepiPred v1.0 Linear Epitope Prediction tool. Results APAP and IB were found to interact with proteins involved in cellular process, metabolism, and virulence. The virulent proteins targeted by the drugs were located in the cytoplasm, which would further add to the effectiveness of the drugs to serve as antimicrobial agents. Finally, epitope prediction revealed multiple epitopes in the virulent proteins which can be specifically focused on. Conclusions APAP and IB were found to target vital proteins involved in the cellular process, metabolism, and virulence of red complex pathogens. An in-depth knowledge on the interaction of these drugs and their antibacterial activity would add to the plethora of merits gained by these drugs in clinical settings. Further in vitro studies on a wide range of pathogens are warranted to substantiate the true interactions between the drugs and the protein repertoire of pathogens.

In silico validation of the non-antibiotic drugs acetaminophen and ibuprofen as antibacterial agents against red complex pathogens

Concern over antibiotic resistance is growing, and new classes of antibiotics, particularly against Gram-negative bacteria, are needed. However, even if the scientific hurdles can be overcome, it could take decades for sufficient numbers of such antibiotics to become available. As an interim solution, antibiotic resistance could be 'broken' by co-administering appropriate non-antibiotic drugs with failing antibiotics. Several marketed drugs that do not currently have antibacterial indications can either directly kill bacteria, reduce the antibiotic minimum inhibitory concentration when used in combination with existing antibiotics and/or modulate host defence through effects on host innate immunity, in particular by altering inflammation and autophagy. This article discusses how such 'antibiotic resistance breakers' could contribute to reducing the antibiotic resistance problem, and analyses a priority list of candidates for further investigation.

Antibiotic resistance breakers: can repurposed drugs fill the antibiotic discovery void?

Fast mineralization and detoxification of amoxicillin and diclofenac by photocatalytic ozonation and application to an urban wastewater

Potential role of non-antibiotics (helper compounds) in the treatment of multidrug-resistant Gram-negative infections: mechanisms for their direct and indirect activities.

Subramanian Annadurai

Papers

Potential management of resistant microbial infections with a novel non-antibiotic: the anti-inflammatory drug diclofenac sodium