Biofilm Formation in Aspergillus fumigatus

Abstract

The first step of pathobiological development of Aspergillus fumigatus following the inhalation of airborne conidia is the colonization of the upper respiratory tract. Modifications of the cell wall during biofilm formation are not unique to A. fumigatus. For a better understanding of biofilm formation in chronic A. fumigatus infections, an A. fumigatus biofilm was produced on human bronchial epithelial cells (16HBE). Several studies have reported that biofilm production aids in the development of antimicrobial drug resistance in C. albicans and bacteria. Persister cells, interactions of the drugs with polysaccharides of the extracellular matrix (ECM), and the ECM acting as a barrier can contribute to reduced antifungal drug susceptibility. In the study by Mowat et al., caspofungin (CSP) demonstrated poor overall activity against adherent multicellular A. fumigatus cells. Itraconazole (ITC) was ineffective against adherent multicellular populations of A. fumigatus. Overall, amphotericin B (AMB) was the most effective antifungal drug against A. fumigatus biofilms at the lowest concentrations, followed by voriconazole (VRC), CSP, and ITC. A. fumigatus can produce in vitro an extracellular hydrophobic matrix with typical characteristics of a biofilm under all static conditions tested: on agar medium, polystyrene, or epithelial cells. Under static conditions the mycelial growth is greater than under shaken submerged conditions. The ECM is composed of galactomannan, α-1,3-glucans, monosaccharides and polyols, melanin, and proteins, including major antigens and hydrophobins. All antifungal drugs are significantly less effective when A. fumigatus is grown under biofilm versus planktonic conditions.