Abstract
We investigated the in vitro and in vivo activities of epigallocatechin-3-gallate (EGCg), a green tea component, against Stenotrophomonas maltophilia (Sm) isolates from cystic fibrosis (CF) patients. In vitro effects of EGCg and the antibiotic colistin (COL) on growth inhibition, survival, and also against young and mature biofilms of S. maltophilia were determined. Qualitative and quantitative changes on the biofilms were assessed by confocal laser scanning microscopy (CLSM). Further, in vivo effects of nebulized EGCg in C57BL/6 and Cftr mutant mice during acute Sm lung infection were evaluated. Subinhibitory concentrations of EGCg significantly reduced not only biofilm formation, but also the quantity of viable cells in young and mature biofilms. CLSM showed that EGCg-exposed biofilms exhibited either a change in total biofilm biovolume or an increase of the fraction of dead cells contained within the biofilm in a dose depended manner. Sm infected wild-type and Cftr mutant mice treated with 1,024 mg/L EGCg by inhalation exhibited significantly lower bacterial counts than those undergoing no treatment or treated with COL. EGCg displayed promising inhibitory and anti-biofilm properties against CF Sm isolates in vitro and significantly reduced Sm bacterial counts in an acute infection model with wild type and CF mice. This natural compound may represent a novel therapeutic agent against Sm infection in CF.
Highlights
Bacterial pathogens are progressively reported as an important cause of high morbidity and mortality rates among patients with cystic fibrosis (CF) [1]
We further evaluated if EGCg could be useful in vivo as a novel natural compound for treatment against acute pulmonary infection caused by Sm1 strain in wild type mice in comparison to COL (Figure 3A)
We demonstrated that wild type (C57BL/6) mice nebulised with EGCg exhibited significantly lower CFU/mL (P = 0.0127) in the lungs compared to untreated and COL-treated (P = 0.0106)
Summary
Bacterial pathogens are progressively reported as an important cause of high morbidity and mortality rates among patients with cystic fibrosis (CF) [1]. One plausible explanation for this increasing resistance is the fact that bacteria can form biofilms, a type of microbial community enveloped by extracellular polymeric substances, in which they are subjected to selective mutational pressures probably induced by repeated antibacterial treatments over the long term [1,3,4,5]. Various CF centers worldwide have reported an increased prevalence of Sm [1] It is a multi-drug resistant, opportunistic pathogen that often causes nosocomial infections (e.g. pneumonia) [13]. This Gram-negative rod is recognized by its ability to form biofilms on abiotic surfaces including glass and plastics like polystyrene, as well as on host tissues such as bronchial epithelial cells [13,14]
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