Abstract
The microbial cell wall plays a crucial role in biofilm formation and drug resistance. cspA encodes a repeat-rich glycophosphatidylinositol-anchored cell wall protein in the pathogenic fungus Aspergillus fumigatus. To determine whether cspA has a significant impact on biofilm development and sensitivity to antifungal drugs in A. fumigatus, a ΔcspA mutant was constructed by targeted gene disruption, and we then reconstituted the mutant to wild type by homologous recombination of a functional cspA gene. Deletion of cspA resulted in a rougher conidial surface, reduced biofilm formation, decreased resistance to antifungal agents, and increased internalization by A549 human lung epithelial cells, suggesting that cspA not only participates in maintaining the integrity of the cell wall, but also affects biofilm establishment, drug response, and invasiveness of A. fumigatus.
Highlights
Aspergillus fumigatus is a major cause of infection in individuals with a compromised immune system, including patients undergoing treatment for leukemia, HIV, or organ transplant, and in those suffering from an underlying disease such as cystic fibrosis [1, 2]
Aspergilloma and invasive aspergillosis are the main forms of A. fumigatus infection, both of which are characterized by high mortality rates (50–95%) and the germination of conidia and subsequent invasion of mycelia into tissues such as human pulmonary alveoli [3]
Deletion of cspA changed colony and conidia morphology, reduced biofilm formation, decreased resistance to antifungal agents, and increased internalization by A549 human lung epithelial cells. These findings suggested that cspA participates in maintaining the integrity of the cell wall, and plays an important role in biofilm establishment, drug resistance, and invasiveness of A. fumigatus
Summary
Aspergillus fumigatus is a major cause of infection in individuals with a compromised immune system, including patients undergoing treatment for leukemia, HIV, or organ transplant, and in those suffering from an underlying disease such as cystic fibrosis [1, 2]. Aspergilloma and invasive aspergillosis are the main forms of A. fumigatus infection, both of which are characterized by high mortality rates (50–95%) and the germination of conidia and subsequent invasion of mycelia into tissues such as human pulmonary alveoli [3]. Under natural conditions, such as in human bodies, most fungal and bacterial pathogens are present as part of a biofilm, which contributes to their decreased response to antibiotics and host immune defenses compared with bacteria in the planktonic state [4]. This presentation is clinically recognized as the primary evidence of biofilm formation by A. fumigatus
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