Phenylacetic acid catabolism modulates virulence factors and drug resistance in Acinetobacter baumannii MCC 2076.

Acinetobacter baumannii has emerged as a major global health threat due to its remarkable ability of resistance, persistence in hostile environments and tolerance to stress conditions. Phenylacetic acid (PAA) catabolism, traditionally known for bacterial metabolic advantage, is now being investigated for its role in the pathogenesis of A. baumannii. This study aims to explore how PAA and its metabolic processes influence the virulence factors and antibiotic resistance of A. baumannii MCC 2076. We examined growth kinetics and PAA utilization to assess the time-dependent breakdown of PAA. In vitro analyses were conducted to evaluate biofilm formation, bacterial surface hydrophobicity, and tolerance to desiccation stress in PAA-catabolizing cells. Our findings revealed a two-fold increase in biofilm formation and an 8% enhancement in bacterial surface adherence. Additionally, we observed an increase in efflux pump activity and a decrease in outer membrane permeability when PAA served as a carbon source. All these factors may be responsible for 2- to 3-fold increase in the minimum inhibitory concentration (MIC) of ciprofloxacin, levofloxacin, ampicillin, and piperacillin. A. baumannii cells with an active paa operon demonstrated a higher survival rate under desiccation stress compared to control cells. RT-qPCR analysis indicated the upregulation of genes such as gacA, csuE, ompA, and adeR, which are associated with virulence related genes like biofilm forming, adherence and antibiotic resistance related genes. The catabolism of PAA is crucial, as its utilization significantly alters the virulence characteristics of A. baumannii MCC 2076. This study provides valuable insights into the PAA catabolic pathway's role in modulating virulence gene expression, potentially offering new therapeutic targets for combating A. baumannii infections.