Abstract
Legionella pneumophila is a Gram-negative, facultative intracellular pathogen that causes severe pneumonia known as Legionnaires’ disease. The bacterium causes disease when contaminated water is aerosolized and subsequently inhaled by individuals, which allows the bacteria to gain access to the lungs, where they infect alveolar macrophages. L. pneumophila is ubiquitous in the environment, where it survives by growing in biofilms, intracellularly within protozoa, and planktonically. Biofilms are a major concern for public health because they provide a protective niche that allows for the continuous leaching of bacteria into the water supply. In addition, biofilms enhance the survival of the bacteria by increasing resistance to temperature fluctuations and antimicrobial agents. Currently, there is little known about biofilm formation and regulation by L. pneumophila. Here, we present evidence of a specific gene, bffA, which appears to be involved in the regulation of motility, biofilm formation, cellular replication, and virulence of L. pneumophila. A strain lacking bffA has an enhanced biofilm formation phenotype, forming biofilms that are both faster and thicker than wild type. Additionally, the knockout strain has significantly reduced motility, enhanced uptake into amoebae, and altered growth kinetics on solid media. Our data suggest a potential role for bffA in signaling pathways that govern changes in growth rate and motility in response to environmental conditions.
Highlights
Academic Editor: Yury BelyiLegionella pneumophila is an opportunistic pathogen and the causative agent of a severe form of pneumonia known as Legionnaires’ Disease
We found that a deletion mutant of lpg1387 has altered growth kinetics on solid media, enhanced uptake into amoebae, decreased flagellar motility, and enhanced biofilm formation compared to wild type L. pneumophila
L. pneumophila ∆bffA Exhibits Altered Growth Kinetics on Solid Medium, but Not in Broth, Compared to Wild-Type bffA is annotated as a putative phosphodiesterase, it appears to be lacking key residues that would be involved in the cleavage of c-di-GMP (Figure S1), suggesting it lacks the ability to cleave c-di-GMP but may still be involved in a signaling pathway that responds to fluctuations in intracellular levels of the second messenger
Summary
Legionella pneumophila is an opportunistic pathogen and the causative agent of a severe form of pneumonia known as Legionnaires’ Disease. The presence of biofilms containing L. pneumophila in domestic water supplies has been identified as a potential cause of drinking water-acquired Legionellosis [10]. Upon deletion of the hnox gene, the bacteria display a hyper-biofilm phenotype, suggesting that hnox is inhibiting the activity of lpg1057 to block biofilm formation. When hnox is deleted, intracellular levels of c-di-GMP increase, leading to the hyper-biofilm phenotype observed. These findings demonstrate the importance of c-di-GMP pathways in L. pneumophila, linking the pathway to biofilm regulation and intracellular survival of this pathogen. Our data suggest that the gene, which we named bffA, is involved in the regulation of motility and biofilm formation in L. pneumophila
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