The Influence of Azithromycin on the Biofilm Formation of <i>Pseudomonas aeruginosa</i> in vitro

Abstract

The influence of azithromycin on biofilm formation by Pseudomonas aeruginosa, a cause of refractory chronic respiratory tract infection, was investigated. Alginic acid produced by a mucoid strain of P. aeruginosa was quantified by high-performance liquid chromatography from colonies growing on an agar medium. Polysaccharides in the biofilm formed on silicon chips by a nonmucoid strain were determined by a tryptophan reaction. The effect of azithromycin was examined at concentrations below the minimum inhibitory concentration (sub-MIC) for each strain. Azithromycin significantly inhibited the production of alginic acid from the mucoid strain at ≥ 1/256 MIC, and the production of exopolysaccharides from the nonmucoid strain at ≥ 1/16 MIC. The inhibition of biofilm formation by azithromycin was also observed by scanning electron microscopy. These findings suggest that azithromycin inhibits biofilm formation by P. aeruginosa at concentrations well below the MIC.

Pseudomonas aeruginosa accentuates epithelial-to-mesenchymal transition in the airway

“…Our group and others have shown that azithromycin treatment can reverse the decline in lung function in some patients with BOS [32][33][34][35]. Azithromycin does not have any significant anti-pseudomonal activity but has been shown to exhibit extensive inhibition of the quorum-sensing systems, diminished virulence factor production and impairment of the oxidative stress response [36][37][38]. However, recent data suggest that although azithromycin exhibits activity against P. aeruginosa biofilms, resistant mutants are readily selected, and tailored anti-pseudomonal therapies may be required to eradicate infection in patients receiving azithromycin treatment [39].…”

Azithromycin for cystic fibrosis

“…In addition, macrolides may have more wide ranging effects on the innate immune system, modulating neutrophil function, reducing the presentation of adhesion molecules and altering expression of nitric oxide synthases [15][16][17]. Finally, macrolides may have more mechanistic effects, reducing airway mucus production and altering the biofilm phenotype of P. aeruginosa [18,19].…”

Inhibition of polysaccharide synthesis by the sinR orthologue PGN_0088 is indirectly associated with the penetration of Porphyromonas gingivalis biofilms by macrolide antibiotics

“…These results show that deleting sinR may not affect macrolide resistance of the cell but may contribute to the resistance of biofilms to macrolides. SubMIC levels of AZM inhibit biofilm formation by Pseudomonas aeruginosa (Ichimiya et al, 1996), Haemophilus influenzae (Starner et al, 2008) and P. gingivalis (Maezono et al, 2011). Furthermore, P. gingivalis biofilm formation, determined using a static Fig.…”