Designing of Antimicrobial compounds and finding their mechanism of inhibition on Pseudomonas aeruginosa by in-silico approach

Tanmai Agasam, Anshul Nigam, Ashwani Sharma

Abstract


Pseudomonas aeruginosa is a common opportunistic pathogen known for causing highly problematic, chronic infections in cystic fibrosis (CF) patient’s lungs. Patients with chronic obstructive pulmonary disease (COPD). Complications from intractable Pseudomonas aeruginosa infections eventually compromise lung function. Particularly in CF patients, resulting in death on average, 38 years old. Pseudomonas aeruginosa has a remarkable ability to resist multiple first line antibiotics, either intrinsically or because of Resistance genes are acquired. When Pseudomonas aeruginosa occurs, it is nearly impossible to eradicate the organism. Many antibiotics have been employed to kill bacteria, but the mechanisms of their activities are still unknown. As a result, determining the mechanism of antimicrobial action of those compounds by analysing their interaction with proteins targets in various pathways is critical. This study focuses on the interaction between the antimicrobial compounds with various proteins of Pseudomonas aeruginosa. A total of 20 protein [1] targets were selected from different pathways of Pseudomonas aeruginosa in this research. Propranolol and N-acetylcysteine were the selected antimicrobial compounds. Propranolol and N-acetylcysteine [2] have multiple target sites with various proteins of Pseudomonas aeruginosa. They have good interaction with the proteins. Homology modelling was performed for some of the proteins to predict the structure of the protein. Binding site residues of all the proteins were found from pdbsum or ProFunc. Docking was performed for all proteins with antimicrobial compounds by use of AUTODOCK VINA. Docking was performed to find out the binding of the compounds with various proteins. Toxicity analysis of the drugs was performed by use of VEGA QSAR. After analysing the results, we found that Propranolol has a stronger binding with proteins of Pseudomonas aeruginosa. Propranolol is not a mutagenic substance. Therefore, it is safer to use Propranolol for treating Pseudomonas disease.

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Agasam ET AL 2022

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