The study looked at how the bacteria Acinetobacter baumannii forms sticky communities called biofilms and tested several chemicals, including the natural peptide LL‑37, to see if they could stop this. They found that LL‑37, along with some antibiotics and tannic acid, lowered the bacteria’s ability to make biofilms, while low doses of another drug, tigecycline, actually made biofilm formation worse. The work mainly shows which genes help the bacteria build biofilms and which compounds can interfere with that process.

<i>Acinetobacter baumannii</i>, an important emerging pathogen of nosocomial infections, is known for its ability to form biofilms. Biofilm formation increases the survival rate of <i>A. baumannii</i> on dry surfaces and may contribute to its persistence in the hospital environment, which increases the probability of nosocomial infections and outbreaks. This study was undertaken to characterize the biofilm production of different strains of <i>A. baumannii</i> and the effects of chemical compounds, especially antibiotics, on biofilm formation. In this study, no statistically significant relationship was observed between the ability to form a biofilm and the antimicrobial susceptibility of the <i>A.&#xa0;baumannii</i> clinical isolates. Biofilm formation caused by <i>A. baumannii</i> ATCC 17978 after gene knockout of two-component regulatory system gene <i>baeR</i>, efflux pump genes <i>emrA/emrB</i> and outer membrane coding gene <i>ompA</i> revealed that all mutant strains had less biofilm formation than the wild-type strain, which was further supported by the images from scanning electron microscopy and confocal laser scanning microscopy. The addition of amikacin, colistin, LL-37 or tannic acid decreased the biofilm formation ability of <i>A. baumannii</i>. In contrast, the addition of lower subinhibitory concentration tigecycline increased the biofilm formation ability of <i>A. baumannii</i>. Minimum biofilm eradication concentrations of amikacin, imipenem, colistin, and tigecycline were increased obviously for both wild type and multidrug resistant clinical strain <i>A.&#xa0;baumannii</i> VGH2. In conclusion, the biofilm formation ability of <i>A. baumannii</i> varied in different strains, involved many genes and could be influenced by many chemical compounds.